CV Lattes
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Universidade Estadual de Campinas (UNICAMP). Centro de Hematologia e Hemoterapia (HEMOCENTRO) (Institutional affiliation for the last research proposal) Birthplace: Inglaterra
Graduated in Biochemistry (Medical), University of Birmingham, UK (1993). Ph.D. (Biochemistry) University of Nottingham (1996). Has experience in Biochemistry, focusing on Biochemistry, specialization in the following subjects: nitric oxide, integrin, eosinophil, inflammation and neutrophil. (Source: Lattes Curriculum)
The proposed Thematic Project "Pathophysiological Mechanisms and Treatment of Red Blood Cell Abnormalities" will be developed by the Red Blood Cell Research Group at the Hematology Center, the Department of Clinical Pathology and the Center for Molecular Biology and Genetic Engineering (CBMEG), UNICAMP, in collaboration with various Brazilian and international researchers. The project aim…
Abstract: Sickle cell disease (SCD) is a group of inherited disorders, caused by mutations in the gene encoding ²-globin. The disease causes alterations in the hemoglobin molecule, resulting in altered red blood cell (RBC) properties and shape, and the destruction of these cells in the circulation, leading to anemia and other complications. The pathophysiological changes incurred from thi…
Intravascular hemolysis, or the destruction of red blood cells, occurs in numerous pathological conditions, including the acquired hemolytic anemias and sickle cell disease, as well as during some transfusion reactions, preeclampsia, and infections, such as those caused by malaria or Clostridium perfringens. Hemolysis results in the release of large amounts of damage-associated molecular …
Angiogenesis is characterized by the formation of new capillaries, from pre-existing vessels. This process plays an important role in the supply of oxygen and nutrients to tissues and the migration of inflammatory cells to sites of inflammation. The angiogenic process involves interactions of various cell types and mediators to establish capillary formation. Endothelial cells are key to t…
The activation of the leukocytes and other inflammatory cells, and their consequent adhesion to the endothelium, play a key role in the initiation and propagation of vascular inflammation and may result in endothelial activation, vascular damage and even obstruction of microcirculatory blood flow with subsequent tissue damage. These mechanisms play a central role in the pathophysiology of…
(Only some records are available in English at this moment)
Sickle cell anemia (SCA) is a hemolytic anemia, caused by the inheritance of hemoglobin S (HbS) in homozygous. Inflammation is a fundamental component of its pathophysiology, and can occur acutely and chronically. In general, numbers and levels of leukocytes and proinflammatory cytokines are high in the disease and these are associated with the clinical severity. In this context, transfor…
Sickle Cell Disease (SCD) is characterized by a single mutation in the ²-globin gene, resulting in abnormal hemoglobin (HbS), which polymerizes under low oxygen concentrations. In situations of low oxygen concentrations, hemoglobin polymerizes and red blood cells assume an elongated sickle-like shape, in an event known as sickling. Angiogenesis is the process of vessel formation from pre-…
Sickle cell anemia (SCA) is a hereditary hematological disease that affects the ²-globin gene. The disease is caused by a single base substitution of an adenine for a thymine in the gene, leading to the synthesis of anomalous hemoglobin S (HbS). At low oxygen concentrations, HbS polymerizes and the erythrocyte adopts a characteristically sickled shape. These red cells display altered phys…
(Only some records are available in English at this moment)
Sickle cell anemia (SCA) is caused by a point mutation in the ²-hemoglobin gene, producing abnormal hemoglobin S (HbS). When deoxygenated, HbS polymerizes, causing the red blood cell to become sickle shaped and to rupture more easily. As a result, the disease is characterized by anemia, intravascular hemolysis and vaso-occlusive disease, which can result in painful vaso-occlusive episodes…
Evidence suggests that haem may represent a novel DAMP. Haem generated by intra and extra-vascular haemolysis activates innate immune cells and non-hematopoietic cells, promoting pro-inflammatory activities, such as leukocyte activation, migration and infiltration, adhesion molecule activation, cytokine release and inflammasome formation. Our data suggest that haem is a potent driver of i…
Sickle cell anemia (SCA) is a hereditary hemoglobinopathy resulted from a mutation in the beta-globin gene. This simple monogenic event is responsible for a systemic disorder of enormous complexity that affects multiple organs. The vaso-occlusive crisis is a major cause of morbidity in SCA and result from the interaction of inflammatory cytokines, activated blood cells and vascular endoth…
(Only some records are available in English at this moment)
| 2 / 2 | Ongoing research grants |
| 13 / 12 | Completed research grants |
| 1 / 1 | Ongoing scholarships in Brazil |
| 23 / 19 | Completed scholarships in Brazil |
| 4 / 4 | Completed scholarships abroad |
| 43 / 38 | All research grants and scholarships |
| Associated processes | |
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
| Publications | 15 |
| Citations | 278 |
| Cit./Article | 18.5 |
| Data from Web of Science | |
PROENCA-FERREIRA, RENATA; BRUGNEROTTO, ANA FLAVIA; GARRIDO, VANESSA TONIN; DOMINICAL, VENINA MARCELA; VITAL, DAIANA MORELLI; REIS RIBEIRO, MARILENE DE FATIMA; DOS SANTOS, MELISSA ERCOLIN; TRAINA, FABIOLA; OLALLA-SAAD, SARA T.; COSTA, FERNANDO FERREIRA; et al. Endothelial Activation by Platelets from Sickle Cell Anemia Patients. PLoS One, v. 9, n. 2, FEB 13 2014. Web of Science Citations: 17. (08/57441-0, 09/54279-0)
SILVEIRA, ANGELICA A. A.; MAHON, OLWYN R.; CUNNINGHAM, CLARE C.; CORR, EMMA M.; MENDONCA, RAFAELA; SAAD, SARA T. O.; COSTA, FERNANDO F.; DUNNE, AISLING; CONRAN, NICOLA. S100A8 acts as an autocrine priming signal for heme-induced human M phi pro-inflammatory responses in hemolytic inflammation. Journal of Leukocyte Biology, v. 106, n. 1, p. 35-43, JUL 2019. Web of Science Citations: 2. (14/23170-1, 12/22048-2, 14/19173-5)
CONRAN, NICOLA; BELCHER, JOHN D.. Inflammation in sickle cell disease. CLINICAL HEMORHEOLOGY AND MICROCIRCULATION, v. 68, n. 2-3, p. 263-299, 2018. Web of Science Citations: 13. (14/19173-5)
TORRES, LIDIANE; CONRAN, NICOLA. Emerging pharmacotherapeutic approaches for the management of sickle cell disease. EXPERT OPINION ON PHARMACOTHERAPY, v. 20, n. 2, p. 173-186, JAN 22 2019. Web of Science Citations: 3. (17/14594-0, 14/00984-3)
ALMEIDA, CAMILA BONONI; SCHEIERMANN, CHRISTOPH; JANG, JUNG-EUN; PROPHETE, COLETTE; COSTA, FERNANDO FERREIRA; CONRAN, NICOLA; FRENETTE, PAUL S.. Hydroxyurea and a cGMP-amplifying agent have immediate benefits on acute vaso-occlusive events in sickle cell disease mice. Blood, v. 120, n. 14, p. 2879-2888, OCT 4 2012. Web of Science Citations: 38. (07/58533-3, 11/50959-7)
LANARO, C.; FRANCO-PENTEADO, C. F.; ALBUQUEQUE, D. M.; SAAD, S. T. O.; CONRAN, N.; COSTA, F. F.. Altered levels of cytokines and inflammatory mediators in plasma and leukocytes of sickle cell anemia patients and effects of hydroxyurea therapy. Journal of Leukocyte Biology, v. 85, n. 2, p. 235-242, Feb. 2009. Web of Science Citations: 93. (08/57895-1, 07/54870-5, 07/50853-9)
PROENCA-FERREIRA, RENATA; FRANCO-PENTEADO, CARLA F.; TRAINA, FABIOLA; SAAD, SARA T. O.; COSTA, FERNANDO F.; CONRAN, NICOLA. Increased adhesive properties of platelets in sickle cell disease: roles for alpha(IIb)beta(3)-mediated ligand binding, diminished cAMP signalling and increased phosphodiesterase 3A activity. British Journal of Haematology, v. 149, n. 2, p. 280-288, APR 2010. Web of Science Citations: 18. (07/50853-9)
ANTONIELLIS SILVEIRA, ANGELICA APARECIDA; DOMINICAL, VENINA MARCELA; VITAL, DAIANA MORELLI; FERREIRA, JR., WILSON ALVES; MARANHAO COSTA, FABIO TRINDADE; WERNECK, CLAUDIO C.; COSTA, FERNANDO FERREIRA; CONRAN, NICOLA. Attenuation of TNF-induced neutrophil adhesion by simvastatin is associated with the inhibition of Rho-GTPase activity, p50 activity and morphological changes. International Immunopharmacology, v. 58, p. 160-165, MAY 2018. Web of Science Citations: 1. (14/19173-5, 12/22048-2, 10/19916-7)
CONRAN, NICOLA; TORRES, LIDIANE. cGMP modulation therapeutics for sickle cell disease. Experimental Biology and Medicine, v. 244, n. 2, p. 132-146, FEB 2019. Web of Science Citations: 4. (17/14594-0, 18/08010-9, 14/00984-3)
ANTONIELLIS SILVEIRA, ANGELICA APARECIDA; DOMINICAL, VENINA MARCELA; ALMEIDA, CAMILA BONONI; CHWEIH, HANAN; FERREIRA, JR., WILSON ALVES; VICENTE, CRISTINA PONTES; MARANHAO COSTA, FABIO TRINDADE; WERNECK, CLAUDIO C.; COSTA, FERNANDO FERREIRA; CONRAN, NICOLA. TNF induces neutrophil adhesion via formin-dependent cytoskeletal reorganization and activation of beta-integrin function. Journal of Leukocyte Biology, v. 103, n. 1, p. 87-98, JAN 2018. Web of Science Citations: 3. (14/19173-5, 12/22048-2, 10/19916-7)
NICOLA CONRAN; CAMILA BONONI ALMEIDA. Hemolytic vascular inflammation: an update. Revista Brasileira de Hematologia e Hemoterapia, v. 38, n. 1, p. 55-57, Fev. 2016. (11/50959-7)
ANTONIELLIS SILVEIRA, ANGELICA APARECIDA; DOMINICAL, VENINA MARCELA; VITAL, DAIANA MORELLI; FERREIRA, JR., WILSON ALVES; MARANHAO COSTA, FABIO TRINDADE; WERNECK, CLAUDIO C.; COSTA, FERNANDO FERREIRA; CONRAN, NICOLA. Attenuation of TNF-induced neutrophil adhesion by simvastatin is associated with the inhibition of Rho-GTPase activity, p50 activity and morphological changes. International Immunopharmacology, v. 58, p. 160-165, MAY 2018. Web of Science Citations: 1. (10/19916-7, 14/19173-5, 12/22048-2)
CONRAN, NICOLA; TORRES, LIDIANE. cGMP modulation therapeutics for sickle cell disease. Experimental Biology and Medicine, v. 244, n. 2, p. 132-146, FEB 2019. Web of Science Citations: 4. (17/14594-0, 18/08010-9, 14/00984-3)
GARRIDO, VANESSA TONIN; SONZOGNI, LAURA; MTATIRO, SIANA NKYA; COSTA, FERNANDO F.; CONRAN, NICOLA; THEIN, SWEE LAY. Association of plasma CD4OL with acute chest syndrome in sickle cell anemia. CYTOKINE, v. 97, p. 104-107, SEP 2017. Web of Science Citations: 10. (08/57441-0, 11/17553-7, 12/22043-0, 12/50582-3)
ALMEIDA, CAMILA BONONI; BOTELHO SOUZA, LUCAS EDUARDO; LEONARDO, FLAVIA COSTA; MARANHAO COSTA, FABIO TRINDADE; WERNECK, CLAUDIO C.; COVAS, DIMAS TADEU; COSTA, FERNANDO FERREIRA; CONRAN, NICOLA. Acute hemolytic vascular inflammatory processes are prevented by nitric oxide replacement or a single dose of hydroxyurea. Blood, v. 126, n. 6, p. 711-720, AUG 6 2015. Web of Science Citations: 38. (11/50959-7)
ANTONIELLIS SILVEIRA, ANGELICA APARECIDA; DOMINICAL, VENINA MARCELA; ALMEIDA, CAMILA BONONI; CHWEIH, HANAN; FERREIRA, JR., WILSON ALVES; VICENTE, CRISTINA PONTES; MARANHAO COSTA, FABIO TRINDADE; WERNECK, CLAUDIO C.; COSTA, FERNANDO FERREIRA; CONRAN, NICOLA. TNF induces neutrophil adhesion via formin-dependent cytoskeletal reorganization and activation of beta-integrin function. Journal of Leukocyte Biology, v. 103, n. 1, p. 87-98, JAN 2018. Web of Science Citations: 3. (10/19916-7, 12/22048-2, 14/19173-5)
(References retrieved automatically from State of São Paulo Research Institutions)
GARRIDO, Vanessa Tonin. Avaliação do papel das citocinas inflamatórias, LIGHT e CD40L, na inflamação mediada por plaquetas na anemia falciforme. Tese (Doutorado) - Faculdade de Ciências Médicas. Universidade Estadual de Campinas. (11/17553-7)
SILVEIRA, Angélica Aparecida Antoniellis. Investigação das propriedades pró-inflamatórias do TNF-"alfa" e do heme em leucócitos "in vitro" e "in vivo". Tese (Doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas. (12/22048-2)
BRITO, Pamela Lara de. Avaliação da pressão arterial e alterações do sistema renina-angiotensina em um modelo animal de anemia falciforme. Dissertação (Mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas. (17/03954-6)
FERREIRA, Renata Proenca. Investigação de adesão plaquetaria na anemia falciforme e o papel dos nucleotideos ciclicos nesta adesão. Dissertação (Mestrado) - Faculdade de Ciências Médicas. Universidade Estadual de Campinas (UNICAMP). (06/58788-9)
DOMINICAL, Venina Marcela. Propriedades adesivas e quimiotáticas dos neutrófilos de pacientes com artrite reumatoide e a influência de diferentes medicações. Dissertação (Mestrado) - Faculdade de Ciências Médicas. Universidade Estadual de Campinas (UNICAMP). (08/51345-0)
DOMINICAL, Venina Marcela. Avaliação das interações heterotípicas de neutrófilos em pacientes com anemia falciforme. Tese (Doutorado) - Faculdade de Ciências Médicas. Universidade Estadual de Campinas. (10/18386-4)
ALMEIDA, Camila Bononi de. Papel dos leucócitos na fisiopatologia da anemia falciforme. Tese (Doutorado) - Faculdade de Ciências Médicas. Universidade Estadual de Campinas (UNICAMP). (07/58533-3)
ALMEIDA, Camila Bononi de. Caracterização das fosfodiesterases (PDE) de GMPc nas celulas de linhagem eritroide e efeitos de drogas inibidoras de PDE na produção de hemoglobina fetal. Dissertação (Mestrado) - Faculdade de Ciências Médicas. Universidade Estadual de Campinas (UNICAMP). (04/10152-3)
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ZORZETTO, Nicola Amanda Conran. Avaliação do efeito do heme na ativação de neutrófilos e plaquetas in vitro. Tese (Doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas. (18/08010-9)
COMPOSIÇÃO FARMACÊUTICA PARA CONTROLE DE VASO-OCLUSÃO E SEUS USOS BR1020120161095 - Albert Einstein College of Medicine of Yeshiva University; Universidade Estadual de Campinas (UNICAMP). Fernando Ferreira Costa; Nicola Conran Zorzetto; Camila Bononi De Almeida; Paul S. Frenette - June 2012, 27