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1.
Transfus Med ; 27(2): 142-146, 2017 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-28111825

RESUMO

BACKGROUND: In the last few decades, various red blood cell (RBC) freezing techniques have been developed and improved to enable the preservation of erythrocytes for future use in pre-transfusion tests in reference immunohaematology laboratories. However, not all these techniques have been sufficiently evaluated for the preservation of blood group antigens. OBJECTIVES: In this study, we evaluated the antigenic pattern of RBCs preserved by droplet freezing in liquid nitrogen in a blood bank context. METHODS: Blood samples were evaluated for the reactivity of blood group antigens after droplet freezing using the non-permeable cryoprotective agent polyvinylpyrrolidone (PVP) and sucrose-dextrose (S + D) solutions. RESULTS: No qualitative changes were observed in RBC reactivity after freezing and thawing for the antigens Fyb , Leb , C, E, Cw , Lua , Lub , Kpa , Kpb and Dia . However, cryopreservation using PVP resulted in a significant increase in reactivity of Fyb antigen on comparing fresh and frozen samples (P < 0·001). CONCLUSION: The establishment of detailed protocols for cryopreservation of RBCs, which take into account the maintenance of antigenic characteristics, is necessary to increase security in pre-transfusion testing using frozen RBCs.


Assuntos
Bancos de Sangue , Antígenos de Grupos Sanguíneos/imunologia , Preservação de Sangue/métodos , Criopreservação/métodos , Crioprotetores/farmacologia , Eritrócitos/imunologia , Antígenos de Grupos Sanguíneos/metabolismo , Eritrócitos/metabolismo , Feminino , Glucose/farmacologia , Humanos , Masculino , Povidona/farmacologia , Sacarose/farmacologia
2.
Clin Transl Oncol ; 20(4): 542-549, 2018 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-28905209

RESUMO

PURPOSE: The fusion gene BCR-ABL has an important role to the progression of chronic myeloid leukemia (CML) and several signaling pathways have been characterized as responsible for the terminal blastic phase (BP). However, the initial phase, the chronic phase (CP), is long lasting and there is much yet to be understood about the critical role of BCR-ABL in this phase. This study aims to evaluate transcriptional deregulation in CD34+ hematopoietic cells (CD34+ cells) from patients with untreated newly diagnosed CML compared with CD34+HC from healthy controls. METHODS: Gene expression profiling in CML-CD34 cells and CD34 cells from healthy controls were used for this purpose with emphasis on five main pathways important for enhanced proliferation/survival, enhanced self-renewal and block of myeloid differentiation. RESULTS: We found 835 genes with changed expression levels (fold change ≥ ±2) in CML-CD34 cells compared with CD34 cells. These include genes belonging to PI3K/AKT, WNT/b-catenin, SHH, NOTCH and MAPK signaling pathways. Four of these pathways converge to MYC activation. We also identified five transcripts upregulated in CD34-CML patients named OSBPL9, MEK2, p90RSK, TCF4 and FZD7 that can be potential biomarkers in CD34-CML-CP. CONCLUSION: We show several mRNAs up- or downregulated in CD34-CML during the chronic phase.


Assuntos
Biomarcadores Tumorais/genética , Leucemia Mielogênica Crônica BCR-ABL Positiva/genética , Transdução de Sinais/genética , Transcriptoma , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Antígenos CD34 , MAP Quinases Reguladas por Sinal Extracelular/genética , MAP Quinases Reguladas por Sinal Extracelular/metabolismo , Feminino , Proteínas Hedgehog/genética , Proteínas Hedgehog/metabolismo , Células-Tronco Hematopoéticas/patologia , Humanos , Leucemia Mielogênica Crônica BCR-ABL Positiva/metabolismo , Leucemia Mielogênica Crônica BCR-ABL Positiva/patologia , Masculino , Pessoa de Meia-Idade , Fosfatidilinositol 3-Quinases/genética , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/genética , Proteínas Proto-Oncogênicas c-akt/metabolismo , Receptores Notch/genética , Receptores Notch/metabolismo , Via de Sinalização Wnt/genética , Adulto Jovem
3.
J Neurosurg ; 47(6): 864-70, 1977 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-925742

RESUMO

Dexamethasone (10-(4)M) was shown to inhibit the growth of human gliomas in culture. This was indicated by the inhibition of incorporation of radioactively labeled thymidine into the deoxyribonucleic acid (DNA) of the cells, and by the increase in the generation time of cells exposed to the drug in vitro. On the other hand, tumors obtained from patients who had received dexamethasone before craniotomy grew considerably faster in vitro than tumors from patients who had not been given the drug before operation.


Assuntos
Astrocitoma/tratamento farmacológico , Neoplasias Encefálicas/tratamento farmacológico , Dexametasona/uso terapêutico , Astrocitoma/metabolismo , Neoplasias Encefálicas/metabolismo , Divisão Celular/efeitos dos fármacos , Células Cultivadas , DNA de Neoplasias/biossíntese , Depressão Química , Dexametasona/farmacologia , Avaliação de Medicamentos , Humanos , RNA Neoplásico/biossíntese
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