53 research outputs found

    Use of the far infrared spectroscopy for NaCl and KCl minerals characterization : a case study of halides from KƂodawa in Poland

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    The paper presents research on chloride minerals of natural origin from KƂodawa (Poland), i.e., colorless, blue and purple halite as well as colorless sylvite. Selected samples of minerals were studied by chemical analysis (ICP-OES, ICP-MS, titration methods) and crystallographic measurements. Then, for the tested halides, research was carried out using far-infrared spectroscopy. Spectroscopic studies confirmed the simple way of distinguishing NaCl and KCl minerals using far-infrared spectroscopy, known in the literature. The novelty is that the article presents for the first time the experimental far infrared spectra of natural blue and purple halite. It was observed that the blue (178 cm−1) and purple (176 cm−1) halites have the strongest infrared band slightly shifted towards higher wavenumbers compared to colorless halite (174 cm−1). As part of the work, the infrared spectra of the crystal structure models of sodium and potassium chloride were calculated for the first time using the density functional theory (with the B3LYP functional and the 6-31G* basis set, 125-atom model). The proposed approach can be used not only as a powerful method differentiating NaCl and KCl minerals, but it can also help with understanding of different defects in crystal lattices for naturally occurring halides and crystals of other minerals

    Transcriptional responses of winter barley to cold indicate nucleosome remodelling as a specific feature of crown tissues

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    We report a series of microarray-based comparisons of gene expression in the leaf and crown of the winter barley cultivar Luxor, following the exposure of young plants to various periods of low (above and below zero) temperatures. A transcriptomic analysis identified genes which were either expressed in both the leaf and crown, or specifically in one or the other. Among the former were genes responsible for calcium and abscisic acid signalling, polyamine synthesis, late embryogenesis abundant proteins and dehydrins. In the crown, the key organ for cereal overwintering, cold treatment induced transient changes in the transcription of nucleosome assembly genes, and especially H2A and HTA11, which have been implicated in cold sensing in Arabidopsis thaliana. In the leaf, various heat-shock proteins were induced. Differences in expression pattern between the crown and leaf were frequent for genes involved in certain pathways responsible for osmolyte production (sucrose and starch, raffinose, Îł-aminobutyric acid metabolism), sugar signalling (trehalose metabolism) and secondary metabolism (lignin synthesis). The action of proteins with antifreeze activity, which were markedly induced during hardening, was demonstrated by a depression in the ice nucleation temperature

    Short ingestion tests as alternative proposal for conventional range finding assays with Thamnocephalus platyurus and Brachionus calyciflorus

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    The goal of this study was to evaluate whether short 1 h sublethal assays may predict the results of 24 h lethality assays with rotifers Brachionus calyciflorus and anostracan crustaceans Thamnocephalus platyurus . The test bionts were hatched from cysts. Inhibition of ingestion was observed after 15 min of incubation of rotifers and crustaceans with the suspension of carmine and latex beads, respectively. Nine compounds with different modes of action were used as toxicants zinc ions, sodium dodecyl sulphate, p-nitrophenol, 3, 5-dichlorophenol and pharmaceuticals propranolol, fluoxetine, abamectin, doramectin and ivermectin. The toxicity values observed in the ingestion tests were very close to the mortality values over a wide range of toxicity from a low toxic surfactant to very toxic avermectins. The ratio between the 1 h EC50’s in the ingestion test and the 24 h LC50’s in the lethality test was below 2 in all cases for rotifers, and 7 in 9 cases for crustaceans. The toxicity of zinc and 3,5-dichlorophenol in the Thamnotoxkit Fℱ was 15-fold higher and 10 fold lower than in the ingestion test, respectively. The 24 h LC50 values are within the range of 25-400 % of the 1 h EC50 values for almost all toxicants tested with the exception of p-nitrophenol for B. calyciflorus and zinc and 3, 5-dichlorophenol for T. platyurus. Short, 1 h ingestion assays Rotoxrapid and Rapidtoxkit are good predictors of the mortality over the next 24 h and can be used as a range finding tests for representatives of pharmaceuticals and surfactants

    Desmopressin treatment improves platelet function under flow in patients with postoperative bleeding

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    Background Patients undergoing major cardiothoracic surgery are subjected to dilution, owing to massive fluid infusion and blood component transfusion. These patients may experience bleeding perioperatively, and are frequently treated with the endothelium-activating agent desmopressin. ObjectivesTo investigate the effect of desmopressin administration on von Willebrand factor (VWF)-dependent coagulant and platelet functions under flow conditions. Patients/methodsBlood from 16 patients with postoperative bleeding was obtained before and after desmopressin treatment (0.3gkg(-1) body weight), and assessed for coagulant properties and platelet function. Furthermore, VWF antigen levels and multimer composition were determined in both samples. ResultsDesmopressin treatment did not change thrombin generation in plasma or whole blood thromboelasticity. Also coagulation factor levels (other than factorVIII) and coagulation times were unchanged, suggesting that desmopressin treatment did not have a major effect on the coagulant activity. On the other hand, desmopressin treatment raised the already high plasma levels of VWF from a median of 116IUmL(-1) (interquartile range [IQR]102-154IUmL(-1)) to a median of 160IUmL(-1) (IQR126-187IUmL(-1)) (P=0.007), owing to accumulation of the high molecular weight VWF multimers. Furthermore, desmopressin treatment caused an increase in collagen-dependent thrombus formation and platelet phosphatidylserine exposure. Markers of thrombus formation correlated with the plasma levels of VWF. Invitro control experiments confirmed a major contribution of VWF to thrombus formation and procoagulant activity under conditions of blood dilution. ConclusionsDesmopressin treatment of patients with bleeding complications after cardiothoracic surgery induces the release of high molecular weight VWF multimers, which enhance platelet activation and thrombus formation under flow conditions

    Tyrosine kinase inhibitor-induced defects in DNA repair sensitize FLT3(ITD)-positive leukemia cells to PARP1 inhibitors

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    Mutations in FMS-like tyrosine kinase 3 (FLT3), such as internal tandem duplications (ITDs), can be found in up to 23% of patients with acute myeloid leukemia (AML) and confer a poor prognosis. Current treatment options for FLT3(ITD)-positive AMLs include genotoxic therapy and FLT3 inhibitors (FLT3i's), which are rarely curative. PARP1 inhibitors (PARP1i's) have been successfully applied to induce synthetic lethality in tumors harboring BRCA1/2 mutations and displaying homologous recombination (HR) deficiency. We show here that inhibition of FLT3(ITD) activity by the FLT3i AC220 caused downregulation of DNA repair proteins BRCA1, BRCA2, PALB2, RAD51, and LIG4, resulting in inhibition of 2 major DNA double-strand break (DSB) repair pathways, HR, and nonhomologous end-joining. PARP1i, olaparib, and BMN673 caused accumulation of lethal DSBs and cell death in AC220-treated FLT3(ITD)-positive leukemia cells, thus mimicking synthetic lethality. Moreover, the combination of FLT3i and PARP1i eliminated FLT3(ITD)-positive quiescent and proliferating leukemia stem cells, as well as leukemic progenitors, from human and mouse leukemia samples. Notably, the combination of AC220 and BMN673 significantly delayed disease onset and effectively reduced leukemia-initiating cells in an FLT3(ITD)-positive primary AML xenograft mouse model. In conclusion, we postulate that FLT3i-induced deficiencies in DSB repair pathways sensitize FLT3(ITD)-positive AML cells to synthetic lethality triggered by PARP1i's. Therefore, FLT3(ITD) could be used as a precision medicine marker for identifying AML patients that may benefit from a therapeutic regimen combining FLT3 and PARP1i's
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