Zobrazení zdroje stránky Andresenblaabjerg3878

canescens responding to drought stress. In addition, the concentration of free proline, bataine and soluble sugars exhibited a significant increase in the presence of NaCl under drought stress, and the betaine contribution to leaf Ψs was significantly increased by additional NaCl compared with that under drought treatment alone, suggesting that compatible solutes are also involved in OA in addition to functioning as protectants to alleviate water deficit injury. Although WRKY transcription factors (TFs) are known to be involved in the regulation of plant root development, the mechanisms by which these TFs regulate plant tolerance to ammonium (NH4+) toxicity remain unclear. To identify the molecular mechanisms underlying NH4+-induced repression of primary root growth and NH4+ sensitivity in Arabidopsis, wild-type (Col-0) and mutant (wrky23) plants were treated with 10&nbsp;mM KNO3 (control) or 5&nbsp;mM (NH4)2SO4 (NH4+ toxicity) for 7 days. Under NH4+ toxicity, the fresh weight of wrky23 mutant was significantly lower than that of Col-0 plants, and the NH4+ concentration in wrky23 roots was significantly higher than that in Col-0 roots. However, we observed no significant differences between the two genotypes under the control treatment. Ammonium transporter AMT1;2 expression was induced in wrky23 roots but not in Col-0 roots. The transcript levels of cytosolic glutamine synthetase-encoding genes and activity of glutamine synthetase did not differ significantly between wrky23 and Col-0. Furthermore, the fluorescence and staining patterns of DR5GFP and DR5GUS, respectively, were more pronounced under NH4+ toxicity than under the control treatment. Collectively, our results indicate that AMT1;2 expression was induced in the wrky23 mutant in response to NH4+ toxicity, leading to NH4+ accumulation in the roots and primary root growth repression. Under NH4+ toxicity, both auxin transport and distribution were affected, and auxin accumulation in the root tips inhibited primary root growth in the wrky23 mutant. Our study provides important insights into the molecular mechanisms by which WRKY23 TF regulates plant responses to NH4+ toxicity. We investigated vanillic acid-induced salt tolerance in tomato by exploring the plant defense systems. Ten-d-old tomato (Solanum lycopersicum L. cv. Pusa Ruby) seedlings were treated with salt (NaCl; 150&nbsp;mM) and vanillic acid (VA; 40 and 50&nbsp;μM) separately and in combination with salt. Salinity restricted seedlings growth, biomass accumulation, chlorophyll and carotenoid contents. Salt-induced osmotic stress was indicated by lower leaf relative water content (RWC) and elevated proline (Pro) content, where higher Na+/K+ ratio indicated the ionic toxicity. Tomato seedlings went through oxidative damage due to acute reactive oxygen species (ROS) production and lipoxygenase (LOX) activity and confirmed by higher lipid peroxidation and membrane damage under salinity. Conversely, exogenous VA reduced osmotic and ionic toxicity in stressed-seedlings by enhancing the RWC and Pro level, and lowering Na+/K+ ratio, respectively. [https://www.selleckchem.com/products/k03861.html AUZ454] Exogenous VA up-regulated the components of antioxidant defense system in salt-treated seedlings resulted in the reduction of ROS production, LOX activity and membrane damage in stressed-seedlings. Additionally, VA application caused the reduction of toxic methylglyoxal accumulation under salt stress through the enhancement of glyoxalase system. Thus, VA-induced alleviation of osmotic, ionic and oxidative stresses leading to improve plant growth and chlorophyll synthesis in stressed-seedlings. So, VA significantly improves salinity tolerance and plant growth performance by involving the actions of plant antioxidant defense and glyoxalase systems. OBJECTIVES The evaluation of disease extent and post-therapy surveillance of head and neck cancer using 2-deoxy-2-[18F]fluoro-d-glucose ([18F]FDG) PET is often complicated by physiological uptake in normal tissues of the head and neck region, especially after surgery or radiotherapy. However, irrespective of low positive predictive values, [18F]FDG PET remains the standard of care to stage the disease and monitor recurrences. Here, we report the preclinical use of a targeted poly (ADP-ribose) polymerase1 (PARP1) binding PET tracer, fluorine-18 labeled poly (ADP-ribose) polymerase1 inhibitor ([18F]PARPi), as a potential alternative with greater specificity. METHODS Using an orthotopic xenograft mouse model injected with either FaDu or Cal 27 (human squamous cell carcinoma cell lines) we performed PET/CT scans with the 2 tracers and compared the results. Gamma counts and autoradiography were also assessed and correlated with histology. RESULTS The average retained activity of [18F]PARPi across cell lines in tumor-bearing tongues was 0.9 ± 0.3%ID/g, 4.1 times higher than in control (0.2 ± 0.04%ID/g). Autoradiography and histology confirmed that the activity arose almost exclusively from the tumor areas, with a signal/normal tissue around a ratio of 42.9 ± 21.4. In vivo, [18F]PARPi-PET allowed delineation of tumor from healthy tissue (p  less then  .005), whereas [18F]FDG failed to do so (p = .209). CONCLUSIONS AND IMPLICATIONS FOR PATIENT CARE We demonstrate that [18F]PARPi is more specific to tongue tumor tissue than [18F]FDG. [18F]PARPi PET allows for the straightforward delineation of oral cancer in mouse models, suggesting that clinical translation could result in improved imaging of head and neck cancer when compared to [18F]FDG. PURPOSE Molecular imaging of cancer cells' reaction to radiation damage can provide a non-invasive measure of tumour response to treatment. The cell surface glycoprotein ICAM-1 (CD54) was identified as a potential radiation response marker. SPECT imaging using an 111In-radiolabelled anti-ICAM-1 antibody was explored. METHODS PSN-1 cells were irradiated (10&nbsp;Gy), and protein expression changes were investigated using an antibody array on cell lysates 24&nbsp;h later. Results were confirmed by western blot, flow cytometry and immunofluorescence. We confirmed the affinity of an 111In-labelled anti-ICAM-1 antibody in vitro, and in vivo, in PSN-1-xenograft bearing mice. The xenografts were irradiated (0 or 10&nbsp;Gy), and [111In]In-anti-ICAM-1 SPECT/CT images were acquired 24, 48 and 72&nbsp;h after intravenous administration. RESULTS ICAM-1 was identified as a potential marker of radiation treatment using an antibody array in PSN-1 cell lysates following irradiation, showing a significant increase in ICAM-1 signal compared to non-irradiated cells.