Evaluation of micro-energy dispersive X-ray fluorescence and histochemical tests for aluminium detection in plants from High Altitude Rocky Complexes, Southeast Brazil

The soils developed under High Altitude Rocky Complexes in Brazil are generally of very low chemical fertility, with low base saturation and high exchangeable aluminium concentration. This stressful condition imposes evolutionary pressures that lead to ecological success of plant species that are able to tolerate or accumulate high amounts of aluminium. Several analytical methods are currently available for elemental mapping of biological structures, such as micro-X-ray fluorescence (μ-EDX) and histochemical tests. The aim of this study was to combine μ-EDX analysis and histochemical tests to quantify aluminium in plants from High Altitude Rocky Complexes, identifying the main sites for Al-accumulation. Among the studied species, five showed total Al concentration higher than 1000 mg kg−1. The main Al-hyperaccumulator plants, Lavoisiera pectinata, Lycopodium clavatum and Trembleya parviflora presented positive reactions in the histochemical tests using Chrome Azurol and Aluminon. Strong positive correlations were observed between the total Al concentrations and data obtained by μ-EDX analysis. The μ-EDX analysis is a potential tool to map and quantify Al in hyperaccumulator species, and a valuable technique due to its non-destructive capacity. Histochemical tests can be helpful to indicate the accumulation pattern of samples before they are submitted for further μ-EDX scrutiny

DataSheet_1_Altered distribution and function of NK-cell subsets lead to impaired tumor surveillance in JAK2V617F myeloproliferative neoplasms.pdf

In cancer, tumor cells and their neoplastic microenvironment can sculpt the immunogenic phenotype of a developing tumor. In this context, natural killer (NK) cells are subtypes of lymphocytes of the innate immune system recognized for their potential to eliminate neoplastic cells, not only through direct cytolytic activity but also by favoring the development of an adaptive antitumor immune response. Even though the protective effect against leukemia due to NK-cell alloreactivity mediated by the absence of the KIR-ligand has already been shown, and some data on the role of NK cells in myeloproliferative neoplasms (MPN) has been explored, their mechanisms of immune escape have not been fully investigated. It is still unclear whether NK cells can affect the biology of BCR-ABL1-negative MPN and which mechanisms are involved in the control of leukemic stem cell expansion. Aiming to investigate the potential contribution of NK cells to the pathogenesis of MPN, we characterized the frequency, receptor expression, maturation profile, and function of NK cells from a conditional Jak2V617F murine transgenic model, which faithfully resembles the main clinical and laboratory characteristics of human polycythemia vera, and MPN patients. Immunophenotypic analysis was performed to characterize NK frequency, their subtypes, and receptor expression in both mutated and wild-type samples. We observed a higher frequency of total NK cells in JAK2V617F mutated MPN and a maturation arrest that resulted in low-numbered mature CD11b+ NK cells and increased immature secretory CD27+ cells in both human and murine mutated samples. In agreement, inhibitory receptors were more expressed in MPN. NK cells from Jak2V617F mice presented a lower potential for proliferation and activation than wild-type NK cells. Colonies generated by murine hematopoietic stem cells (HSC) after mutated or wild-type NK co-culture exposure demonstrated that NK cells from Jak2V617F mice were deficient in regulating differentiation and clonogenic capacity. In conclusion, our findings suggest that NK cells have an immature profile with deficient cytotoxicity that may lead to impaired tumor surveillance in MPN. These data provide a new perspective on the behavior of NK cells in the context of myeloid malignancies and can contribute to the development of new therapeutic strategies, targeting onco-inflammatory pathways that can potentially control transformed HSCs.</p