Acute Lymphoblastic Leukemia (ALL) is the most frequent cancer in pediatric population. Although the treatment has improved and almost 85% of the children are cured about 20% suffer relapse, therefore finding molecules that participate in the pathogenesis of the disease for the identification of relapse and patients at risk is an urgent unmet need. Class I myosins are molecular motors involved in membrane tension, endocytosis, phagocytosis and cell migration and recently they have been shown important for development and aggressiveness of diverse cancer types, however Myo1g an hematopoietic specific myosin has not been studied in cancer so far. We evaluated the expression of Myo1g by qRT-PCR, Immunocytochemistry and Immunofluorescence in a cohort of 133 ALL patients and correlated the expression at diagnosis and after treatment with clinical features and treatment outcomes. We found high expression levels of Myo1g in Peripheral Blood Mononuclear Cells (PBMCs) from patients with ALL at diagnosis and those levels decreased after complete remission; furthermore, we found an increase in Myo1g expression on patients with 9:22 translocation and those who relapse. This study show that Myo1g is over expressed in ALL and that may participate in the pathogenesis of the disease specially in high-risk patients.
In the adaptive immune response, the types of cytokines produced define whether there is a cellular (T1) or a humoral (T2) response. Specifically, in the T1 response, interleukin 2 (IL-2), interferon γ (IFN-γ) and tumor necrosis factor β (TNF-β) are produced, whereas in the T2 response, IL-4, IL-5, IL- 6, IL-10 and IL-13 are primarily produced. Cytokines are primarily involved in the regulation of immune system cells. The aim of the present study was to evaluate the cytokine patterns (Type 1/Type 2) and TNF-α expression levels in children with severe gastrointestinal and respiratory bacterial infections. The enzyme-linked immunosorbent assay (ELISA) technique was used to identify the cytokines and the infectious agents. The results obtained demonstrated that, in general, children with bacterial infections experienced an increase in IL-2, IFN-γ and IL-4 concentrations and a decrease in TNF-α, IL-5 and IL-6 concentrations when compared to healthy children. Specifically, type 1 cytokines and an increased TNF-α concentration were found in children with gastrointestinal infections. However, patients with respiratory infections showed increased concentrations of both T2 (IL-4, IL-6 and IL-10) and T1 (IL-2 and IFN-γ) components. Thus, it was concluded that children with gastrointestinal infections exclusively developed a T1 response, whereas children with respiratory infections developed a T1/T2 response to fight the infection.
Infections in infants and children under five years of age are a public health in México and are one of the major causes of death. Methods In this study, lymphocyte immunophenotyping for CD3+ (T-cells), CD3+CD4+, CD3+CD8+, CD3+CD19+, CD3+CD16/56+, CD45RA+, CD45RO+, CD62L− and CD28− were determined in the whole blood of gastrointestinal and respiratory bacterial infected children, using a fourcolor flow cytometry technique. Results: Our data showed that the percentages and the absolute numbers of monocytes and granulocytes are increased in infected children, when compared to the control group. Similarly, we observed increases in the percentages of B lymphocytes, CD8+ cells, memory T cells (CD4+CD45RO+ and CD8+CD45RO+) and effector lymphocytes (CD4+CD62L− and CD8+CD28−) in infected children compared with the control group. In contrast, naive T cells were decreased in the bacterial infected children relative to the control group. Additionally, we used ELISA assays to identify the pathogen agent in gastrointestinal and respiratory infection.
La asimilación deficiente de alimentos por el organismo conduce a un estado patológico con distintos grados y manifestaciones clínicas, conocido como desnutrición. En los últimos años ha surgido un nuevo ensayo in vivo de detección de mutación somática basado en el gen glucosilfosfatidilinositol de clase A (Pig-a). Este gen es necesario para la síntesis de glicosilfosfatidilinositol (GPI) que une proteínas específicas a la superficie de la célula. Cuando ocurre una mutación en Pig-a, no se puede sintetizar el GPI, ya que, las proteínas no se encuentran en la membrana celular, dando origen al fenotipo GPI negativo, el cual es de fácil detección por medio del análisis con citometría de flujo. En este estudio se utilizó el ensayo Pig-a para examinar el daño génico en ratas desnutridas expuestas al mutágeno N-etil-N-nitrosourea (ENU). Se efectuó el marcaje diferencial de reticulocitos (RET) y eritrocitos (E) de sangre periférica de rata de la cepa Wistar. Se tomó como indicador de daño al material genético de las células, el incremento en las frecuencias de mutantes (FM) Pig-a, que fueron analizadas en un 1 X 106 células, durante 8 semanas. Los resultados muestran que la desnutrición grave por sí misma tiene un efecto dañino sobre la integridad del material genético. La frecuencia de mutantes se incrementó con base en la dosis de ENU y el tiempo de exposición en los grupos con desnutrición (DN).
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