Browsing by Author "Santos, A."
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- Avaliação da hiperalgesia em relação com a administração peri-operatória de opióidesPublication . Brás, A.; Carvalho, A.; Carvalho, C.; Carvalho, M.; Dias, J.; Duarte, A.; Mendes, D.; Mendes, T.; Mesquita, M.; Pinto, A.; Santos, A.; Alves, S.; Amorim, P.
- CD56-Negative Aggressive NK Cell Leukemia Relapsing as Multiple Cranial Nerve Palsies: Case Report and Literature ReviewPublication . Guerreiro, M.; Príncipe, F.; Teles, M.; Fonseca, S.; Santos, A.; Fonseca, E.; Gomes, P.; Marques, C.; Lima, M.Aggressive natural killer cell leukemia (ANKL) is extremely rare and habitually manifests as a systemic disease with multiorgan failure that rapidly evolves to death. The neoplastic natural killer (NK) cells usually harbor the Epstein-Barr virus (EBV) with a latent viral infection pattern type II; they often have a cytoplasmic CD3ε+ and surface CD3-, CD2+, and CD56+ immunophenotype, and they show complex genetic abnormalities affecting multiple tumor suppressor genes and oncogenes. We present a rare case of CD56-negative ANKL and review the clinical and laboratorial criteria for the diagnosis, as well as the available therapies.
- Chemokine Receptor Expression on Normal Blood CD56(+) NK-Cells Elucidates Cell Partners That Comigrate during the Innate and Adaptive Immune Responses and Identifies a Transitional NK-Cell PopulationPublication . Lima, M.; Leander, M.; Santos, M.; Santos, A.; Lau, C.; Queirós, M.; Gonçalves, M.; Fonseca, S.; Moura, J.; Teixeira, M.; Orfao, A.Studies of chemokine receptors (CKR) in natural killer- (NK-) cells have already been published, but only a few gave detailed information on its differential expression on blood NK-cell subsets. We report on the expression of the inflammatory and homeostatic CKR on normal blood CD56(+low) CD16(+) and CD56(+high) CD16(-/+low) NK-cells. Conventional CD56(+low) and CD56(+high) NK-cells present in the normal PB do express CKR for inflammatory cytokines, although with different patterns CD56(+low) NK-cells are mainly CXCR1/CXCR2(+) and CXCR3/CCR5(-/+), whereas mostly CD56(+high) NK-cells are CXCR1/CXCR2(-) and CXCR3/CCR5(+). Both NK-cell subsets have variable CXCR4 expression and are CCR4(-) and CCR6(-). The CKR repertoire of the CD56(+low) NK-cells approaches to that of neutrophils, whereas the CKR repertoire of the CD56(+high) NK-cells mimics that of Th1(+) T cells, suggesting that these cells are prepared to migrate into inflamed tissues at different phases of the immune response. In addition, we describe a subpopulation of NK-cells with intermediate levels of CD56 expression, which we named CD56(+int) NK-cells. These NK-cells are CXCR3/CCR5(+), they have intermediate levels of expression of CD16, CD62L, CD94, and CD122, and they are CD57(-) and CD158a(-). In view of their phenotypic features, we hypothesize that they correspond to a transitional stage, between the well-known CD56(+high) and CD56(+low) NK-cells populations.
- CHEMOKINE RECEPTOR REPERTOIRE REFLECTS MATURE T-CELL LYMPHOPROLIFERATIVE DISORDER CLINICAL PRESENTATIONPublication . Moura, J.; Rodrigues, J.; Santos, A.; Teixeira, M.; Queirós, M.; Santos, M.; Gonçalves, M.; Fonseca, S.; Laranjeira, C.; Ribeiro, F.; Acosta, M.; Rodrigues, A.; Júnior, E.; Lima, M.The World Health Organisation classification of mature T-cell lymphoproliferative disorders, combines clinical, morphological and immunophenotypic data. The later majorly contributes for the classification, as well as to the understanding of the malignant T-cell behaviour. The fact that T-cell migration is regulated by chemokines should, in theory, enable us to identify tissue tropism and organ involvement by neoplastic Tcells, through monitoring of chemokine receptor surface expression.
- CONTRIBUTO DA CITOMETRIA DE FLUXO PARA O ESTUDO DOS RETICULÓCITOSPublication . Queirós, M.; Moreira, S.; Leander, M.; Freitas, I.; Cleto, E.; Santos, F.; Henriques, M.; Teixeira, F.; Iglésias, I.; Santos, A.; Santos, M.; Gonçalves, M.; Fonseca, S.; Lau, C.; Bini-Antunes, M.; Teixeira, M.; Pinho, L.; Santos-Silva, A.; Lima, M.Os reticulócitos são eritrócitos jovens cuja presença no sangue periférico (SP) reflecte a actividade eritropoiética da medula óssea. Assim e apesar de, em determinadas situações de stress ou em diversas patologias hematológicas, se poderem encontrar no SP reticulócitos em diferentes estadios de maturação,pouco se sabe acerca deles. Este trabalho teve como objectivo caracterizar fenotipicamente as várias fases de maturação dos reticulócitos por citometria de fluxo (CF).
- Economic Impact of Prosthetic Joint Infection - an Evaluation Within the Portuguese National Health SystemPublication . Sousa, A.; Carvalho, A.; Pereira, C.; Reis, E.; Santos, A.; Abreu, M.; Soares, D.; Fragoso, R.; Ferreira, S.; Reis, M.; Sousa, R.Introduction: Prosthetic infection is a devastating complication of arthroplasty and carries significant economic burden. The objective of this study was to analyze the economic impact of prosthetic hip and knee infection in Portuguese National Health System. Material and Methods: Case-control study carried out from January 2014 to December 2015. The mean costs of primary arthroplasties and prosthetic revision surgeries for non-infectious reasons were compared with the costs of prosthetic infections treated with debridement and preservation of the prosthesis or with two-stage exchange arthroplasty.The reimbursement for these cases was also evaluated and compared with its real costs. Results: A total of 715 primary arthroplasties, 35 aseptic revisions, 16 surgical debridements and 15 revisions for infectious reasons were evaluated. The cost of primary arthroplasties was 3,230€ in the hips and 3,618€ in the knees. The cost of aseptic revision was 6,089€ in the hips and 7,985€ in the knees. In the cases treated with debridement and implant retention the cost was 5,528€ in the hips and 4,009€ in the knees. In cases of infections treated with a two-stage revision the cost was 11,415€ and 13,793€ for hips and knees, respectively. Conclusion: As far as we know this is the first study that analyzes the economic impact of prosthetic infection in the Portuguese context. Although direct compensation for treating infected cases is much lower than calculated costs, infected cases push the overall hospital case-mix-index upwards thus increasing financial compensation for the entire cohort of treated patients. This knowledge will allow for more informed decisions about health policies in the future.
- Expressão dos recetores de quimiocinas, CXCR3 e CCR5, nas células natural killer do sangue de cordão umbilicalPublication . Bini-Antunes, M.; Leander, M.; Rebelo, R.; Benevides, P.; Santos, A.; Rodrigues, J.; Oliveira, L.; Queirós, M.; Santos, M.; Gonçalves, M.; Fonseca, S.; Lau, C.; Teixeira, M.; Lima, M.
- Gastroenteropancreatic Neuroendocrine Neoplasia Characterization in Portugal: Results from the NETs Study Group of the Portuguese Society of Endocrinology, Diabetes and MetabolismPublication . Santos, A.; Vinagre, J.; Soares, P.; Claro, I.; Sanches, A.; Gomes, L.; Fernandes, I.; Catarino, A.; Preto, J.; Pereira, B.; Marques, A.; Rodrigues, F.; Amaral, C.; Rocha, G.; Mellidez, J.; Simões, H.; Lopes, J.; Bugalho, M.Background: The incidence of gastroenteropancreatic neuroendocrine neoplasms (GEP-NENs) has been increasing in the last five decades, but there is no large-scale data regarding these tumours in Portugal. We conducted a cross-sectional, multicentric study in main Portuguese centers to evaluate the clinical, pathological, and therapeutic profile of GEP-NENs. Methods: From November, 2012, to July, 2014, data from 293 patients diagnosed with GEP-NENs from 15 centers in Portugal was collected and registered in an online electronic platform. Results: Median age at diagnosis was 56.5 (range: 15-87) years with a preponderance of females (54.6%). The most frequent primary sites were the pancreas (31.1%), jejunum-ileum (24.2%), stomach (13.7%), and rectum (8.5%). Data regarding hormonal status was not available in most patients (82.3%). Stratified by the tumour grade (WHO 2010 classification), we observed 64.0% of NET G1, 24.7% of NET G2, and 11.3% of NEC. Poorly differentiated tumours occurred mainly in older patients (p = 0.017), were larger (p < 0.001), and presented more vascular (p = 0.004) and lymphatic (p = 0.001) invasion. At the time of diagnosis, 44.4% of GEP-NENs presented metastatic disease. Surgery (79.6%) and somatostatin analogues (30.7%) were the most frequently used therapies of GEP-NENs with reported grading. Conclusion: In general, Portuguese patients with GEP-NENs presented similar characteristics to other populations described in the literature. This cross-sectional study represents the first step to establish a national database of GEP-NENs that may aid in understanding the clinical and epidemiological features of these tumours in Portugal. Methods: From November, 2012, to July, 2014, data from 293 patients diagnosed with GEP-NENs from 15 centers in Portugal was collected and registered in an online electronic platform. Results: Median age at diagnosis was 56.5 (range: 15-87) years with a preponderance of females (54.6%). The most frequent primary sites were the pancreas (31.1%), jejunum-ileum (24.2%), stomach (13.7%), and rectum (8.5%). Data regarding hormonal status was not available in most patients (82.3%). Stratified by the tumour grade (WHO 2010 classification), we observed 64.0% of NET G1, 24.7% of NET G2, and 11.3% of NEC. Poorly differentiated tumours occurred mainly in older patients (p = 0.017), were larger (p < 0.001), and presented more vascular (p = 0.004) and lymphatic (p = 0.001) invasion. At the time of diagnosis, 44.4% of GEP-NENs presented metastatic disease. Surgery (79.6%) and somatostatin analogues (30.7%) were the most frequently used therapies of GEP-NENs with reported grading. Conclusion: In general, Portuguese patients with GEP-NENs presented similar characteristics to other populations described in the literature. This cross-sectional study represents the first step to establish a national database of GEP-NENs that may aid in understanding the clinical and epidemiological features of these tumours in Portugal.
- Genetic disruption of NRF2 promotes the development of necroinflammation and liver fibrosis in a mouse model of HFE-hereditary hemochromatosisPublication . Duarte, T.; Caldas, C.; Santos, A.; Silva-Gomes, S.; Santos-Gonçalves, A.; Martins, M.; Porto, G.; Lopes, J.In hereditary hemochromatosis, iron deposition in the liver parenchyma may lead to fibrosis, cirrhosis and hepatocellular carcinoma. Most cases are ascribed to a common mutation in the HFE gene, but the extent of clinical expression is greatly influenced by the combined action of yet unidentified genetic and/or environmental modifying factors. In mice, transcription factor NRF2 is a critical determinant of hepatocyte viability during exposure to acute dietary iron overload. We evaluated if the genetic disruption of Nrf2 would prompt the development of liver damage in Hfe(-/-) mice (an established model of human HFE-hemochromatosis).
- Hepcidin is regulated by promoter-associated histone acetylation and HDAC3Publication . Pasricha, S.; Lim, P.; Duarte, T.; Casu, C.; Oosterhuis, D.; Mleczko-Sanecka, K.; Suciu, M.; Da Silva, A.; Al-Hourani, K.; Arezes, J.; McHugh, K.; Gooding, S.; Frost, J.; Wray, K.; Santos, A.; Porto, G.; Repapi, E.; Gray, N.; Draper, S.; Ashley, N.; Soilleux, E.; Olinga, P.; Muckenthaler, M.; Hughes, J.; Rivella, S.; Milne, T.; Armitage, A.; Drakesmith, H.Hepcidin regulates systemic iron homeostasis. Suppression of hepcidin expression occurs physiologically in iron deficiency and increased erythropoiesis but is pathologic in thalassemia and hemochromatosis. Here we show that epigenetic events govern hepcidin expression. Erythropoiesis and iron deficiency suppress hepcidin via erythroferrone-dependent and -independent mechanisms, respectively, in vivo, but both involve reversible loss of H3K9ac and H3K4me3 at the hepcidin locus. In vitro, pan-histone deacetylase inhibition elevates hepcidin expression, and in vivo maintains H3K9ac at hepcidin-associated chromatin and abrogates hepcidin suppression by erythropoietin, iron deficiency, thalassemia, and hemochromatosis. Histone deacetylase 3 and its cofactor NCOR1 regulate hepcidin; histone deacetylase 3 binds chromatin at the hepcidin locus, and histone deacetylase 3 knockdown counteracts hepcidin suppression induced either by erythroferrone or by inhibiting bone morphogenetic protein signaling. In iron deficient mice, the histone deacetylase 3 inhibitor RGFP966 increases hepcidin, and RNA sequencing confirms hepcidin is one of the genes most differentially regulated by this drug in vivo. We conclude that suppression of hepcidin expression involves epigenetic regulation by histone deacetylase 3.Hepcidin controls systemic iron levels by inhibiting intestinal iron absorption and iron recycling. Here, Pasricha et al. demonstrate that the hepcidin-chromatin locus displays HDAC3-mediated reversible epigenetic modifications during both erythropoiesis and iron deficiency.
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