Nonannual tree rings in a climate-sensitive Prioria copaifera chronology in the Atrato River, Colombia

In temperate climates, tree growth dormancy usually ensures the annual nature of tree rings, but in tropical environments, determination of annual periodicity can be more complex. The purposes of the work are as follows: (1) to generate a reliable tree‐ring width chronology for Prioria copaifera Griseb. (Leguminoceae), a tropical tree species dwelling in the Atrato River floodplains, Colombia; (2) to assess the climate signal recorded by the tree‐ring records; and (3) to validate the annual periodicity of the tree rings using independent methods. We used standard dendrochronological procedures to generate the P. copaifera tree‐ring chronology. We used Pearson correlations to evaluate the relationship of the chronology with the meteorological records, climate regional indices, and gridded precipitation/sea surface temperature products. We also evaluated 24 high‐precision 14C measurements spread over a range of preselected tree rings, with assigned calendar years by dendrochronological techniques, before and after the bomb spike in order to validate the annual nature of the tree rings. The tree‐ring width chronology was statistically reliable, and it correlated significantly with local records of annual and October–December (OND) streamflow and precipitation across the upper river watershed (positive), and OND temperature (negative). It was also significantly related to the Oceanic Niño Index, Pacific Decadal Oscillation, and the Southern Oscillation Index, as well as sea surface temperatures over the Caribbean and the Pacific region. However, 14C high‐precision measurements over the tree rings demonstrated offsets of up to 40 years that indicate that P. copaifera can produce more than one ring in certain years. Results derived from the strongest climate–growth relationship during the most recent years of the record suggest that the climatic signal reported may be due to the presence of annual rings in some of those trees in recent years. Our study alerts about the risk of applying dendrochronology in species with challenging anatomical features defining tree rings, commonly found in the tropics, without an independent validation of annual periodicity of tree rings. High‐precision 14C measurements in multiple trees are a useful method to validate the identification of annual tree rings

A Europium(III) Complex with an Unusual Anion–Cation Interaction: A Luminescent Molecular Thermometer for Ratiometric Temperature Sensing

This work was supported by the Associated Laboratory for Sustainable Chemistry‐Clean Processes and Technologies – LAQV which is financed by national funds from FCT/MEC (UID/QUI/50006/2019) and co‐financed by the ERDF under the PT2020 Partnership Agreement (POCI‐01‐0145‐FEDER – 007265) The NMR spectrometers are part of The National NMR Facility, supported by Fundação para a Ciência e a Tecnologia (RECI/BBB‐BQB/0230/2012). We also thank to RNEM – Portuguese Mass Spectrometry Network, ref. LISBOA‐01‐0145‐FEDER‐022125, supported by FCT and Lisboa Regional Operational Programme (Lisboa2020). This work has been supported by Fundação para a Ciência e a Tecnologia through the contract n° IST‐ID/077/2018 (Bernardo Monteiro), SFRH/BD/120985/2016 (Mani Outis). Cláudia C. L. Pereira thanks to Fundação para a Ciência e a Tecnologia, MCTES, for the Norma transitória DL 57/2016 Program Contract.An unusual thermally sensitive anion–cation interaction, which is characteristic of the anion [Eu(FOD)4]−, occurs in the complex [CHOL][Eu(FOD)4] (1; CHOL=choline; FOD=1,1,1,2,2,3,3-heptafluoro-7,7-dimethyl-4,6-octanedionate) and affects both quantum yield and thermochromic behavior. This prompted the design of an Eu3+-based ratiometric thermometer that functions at temperatures up to 95 °C through a thermally excited state absorption of the Eu3+ ion. The reusable temperature-sensitive luminescent complex showed a range of relative sensitivity between 0.45 % C−1 at 25 °C, with an increase to 7.0 % C−1 at 95 °C. Confinement of compound 1 in a transparent film of polysulfone resulted in a higher thermal stability of 1 while its luminescence showed a strong temperature dependence.authorsversionpublishe

Neurohormonal activation induces intracellular iron deficiency and mitochondrial dysfunction in cardiac cells

Cèl·lula cardíaca; Deficiència de ferro; Activació neurohormonalCardiac cell; Iron deficiency; Neurohormonal activationCélula cardíaca; Deficiencia de hierro; Activación neurohormonalBackground Iron deficiency (ID) is common in patients with heart failure (HF) and is associated with poor outcomes, yet its role in the pathophysiology of HF is not well-defined. We sought to determine the consequences of HF neurohormonal activation in iron homeostasis and mitochondrial function in cardiac cells. Methods HF was induced in C57BL/6 mice by using isoproterenol osmotic pumps and embryonic rat heart-derived H9c2 cells were subsequently challenged with Angiotensin II and/or Norepinephrine. The expression of several genes and proteins related to intracellular iron metabolism were assessed by Real time-PCR and immunoblotting, respectively. The intracellular iron levels were also determined. Mitochondrial function was analyzed by studying the mitochondrial membrane potential, the accumulation of radical oxygen species (ROS) and the adenosine triphosphate (ATP) production. Results Hearts from isoproterenol-stimulated mice showed a decreased in both mRNA and protein levels of iron regulatory proteins, transferrin receptor 1, ferroportin 1 and hepcidin compared to control mice. Furthermore, mitoferrin 2 and mitochondrial ferritin were also downregulated in the hearts from HF mice. Similar data regarding these key iron regulatory molecules were found in the H9c2 cells challenged with neurohormonal stimuli. Accordingly, a depletion of intracellular iron levels was found in the stimulated cells compared to non-stimulated cells, as well as in the hearts from the isoproterenol-induced HF mice. Finally, neurohormonal activation impaired mitochondrial function as indicated by the accumulation of ROS, the impaired mitochondrial membrane potential and the decrease in the ATP levels in the cardiac cells. Conclusions HF characteristic neurohormonal activation induced changes in the regulation of key molecules involved in iron homeostasis, reduced intracellular iron levels and impaired mitochondrial function. The current results suggest that iron could be involved in the pathophysiology of HF.This work was funded by the following Grants: unrestricted grant from Vifor Pharma and Basic Research Competitive Grant in Cardiology from the Spanish Society of Cardiology 2015

Selection of endogenous genes for gene expression studies in Eucalyptus under biotic (Puccinia psidii) and abiotic (acibenzolar-S-methyl) stresses using RT-qPCR

<p>Abstract</p> <p>Background</p> <p>Rust caused by <it>Puccinia psidii </it>Winter has been limiting for the establishment of new <it>Eucalyptus </it>plantations, as well as for resprouting of susceptible genetic materials. Identifying host genes involved in defense responses is important to elucidate resistance mechanisms. Reverse transcription-quantitative PCR is the most common method of mRNA quantitation for gene expression analysis. This method generally employs a reference gene as an internal control to normalize results. A good endogenous control transcript shows minimal variation due to experimental conditions.</p> <p>Findings</p> <p>We analyzed the expression of 13 genes to identify transcripts with minimal variation in leaves of 60-day-old clonal seedlings of two <it>Eucalyptus </it>clones (rust-resistant and susceptible) subjected to biotic (<it>P. psidii</it>) and abiotic (acibenzolar-S-methyl, ASM) stresses.</p> <p>Conclusions</p> <p>For tissue samples of clones that did not receive any stimulus, a combination of the <it>eEF2 </it>and <it>EglDH </it>genes was the best control for normalization. When pathogen-inoculated and uninoculated plant samples were compared, <it>eEF2 </it>and <it>UBQ </it>together were more appropriate as normalizers. In ASM-treated and untreated leaves of both clones, transcripts of the <it>CYP </it>and <it>elF4B </it>genes combined were the ones with minimal variation. Finally, when comparing expression in both clones for ASM-treated leaves, <it>P. psidii</it>-inoculated leaves, ASM-treated plus <it>P. psidii</it>-inoculated leaves, and their respective controls, the genes with the most stable expression were <it>EgIDH </it>and <it>UBQ</it>. The chitinase gene, which is highly expressed in studies on plant resistance to phytopathogens, was used to confirm variation in gene expression due to the treatments.</p

Sorafenib sensitizes hepatocellular carcinoma cells to physiological apoptotic stimuli

Sorafenib increases survival rate of patients with advanced hepatocellular carcinoma (HCC). The mechanism underlying this effect is not completely understood. In this work we have analyzed the effects of sorafenib on autocrine proliferation and survival of different human HCC cell lines. Our results indicate that sorafenib in vitro counteracts autocrine growth of different tumor cells (Hep3B, HepG2, PLC-PRF-5, SK-Hep1). Arrest in S/G2/M cell cycle phases were observed coincident with cyclin D1 down-regulation. However, sorafenib's main anti-tumor activity seems to occur through cell death induction which correlated with caspase activation, increase in the percentage of hypodiploid cells, activation of BAX and BAK and cytochrome c release from mitochondria to cytosol. In addition, we observed a rise in mRNA and protein levels of the pro-apoptotic BH3-domain only PUMA and BIM, as well as decreased protein levels of the anti-apoptotic MCL1 and survivin. PUMA targeting knock-down, by using specific siRNAs, inhibited sorafenib-induced apoptotic features. Moreover, we obtained evidence suggesting that sorafenib also sensitizes HCC cells to the apoptotic activity of transforming growth factor-beta (TGF-beta) through the intrinsic pathway and to tumor necrosis factor-a (TNF) through the extrinsic pathway. Interestingly, sensitization to sorafenib-induced apoptosis is characteristic of liver tumor cells, since untransformed hepatocytes did not respond to sorafenib inducing apoptosis, either alone or in combination with TGF-beta or TNF. Indeed, sorafenib effectiveness in delaying HCC late progression might be partly related to a selectively sensitization of HCC cells to apoptosis by disrupting autocrine signals that protect them from adverse conditions and pro-apoptotic physiological cytokines. J. Cell. Physiol. 227: 1319-1325, 2012. (C) 2011 Wiley Periodicals, Inc

Flowing Between Fermionic Fixed Points

We study holographic Wilsonian renormalization group flows for bulk spinor fields in AdS. We use this to compute the all-loop beta function for fermionic double trace operators in the dual conformal field theory.Comment: 21 pages. V2: Acknowledgement added; v3: Typo correcte

New genes of Xanthomonas citri subsp. citri involved in pathogenesis and adaptation revealed by a transposon-based mutant library

<p>Abstract</p> <p>Background</p> <p>Citrus canker is a disease caused by the phytopathogens <it>Xanthomonas citri </it>subsp. <it>citri</it>, <it>Xanthomonas fuscans </it>subsp. <it>aurantifolli </it>and <it>Xanthomonas alfalfae </it>subsp. <it>citrumelonis</it>. The first of the three species, which causes citrus bacterial canker type A, is the most widely spread and severe, attacking all citrus species. In Brazil, this species is the most important, being found in practically all areas where citrus canker has been detected. Like most phytobacterioses, there is no efficient way to control citrus canker. Considering the importance of the disease worldwide, investigation is needed to accurately detect which genes are related to the pathogen-host adaptation process and which are associated with pathogenesis.</p> <p>Results</p> <p>Through transposon insertion mutagenesis, 10,000 mutants of <it>Xanthomonas citri </it>subsp. <it>citri </it>strain 306 (Xcc) were obtained, and 3,300 were inoculated in Rangpur lime (<it>Citrus limonia</it>) leaves. Their ability to cause citrus canker was analyzed every 3 days until 21 days after inoculation; a set of 44 mutants showed altered virulence, with 8 presenting a complete loss of causing citrus canker symptoms. Sequencing of the insertion site in all 44 mutants revealed that 35 different ORFs were hit, since some ORFs were hit in more than one mutant, with mutants for the same ORF presenting the same phenotype. An analysis of these ORFs showed that some encoded genes were previously known as related to pathogenicity in phytobacteria and, more interestingly, revealed new genes never implicated with <it>Xanthomonas </it>pathogenicity before, including hypothetical ORFs. Among the 8 mutants with no canker symptoms are the <it>hrpB4 </it>and <it>hrpX </it>genes, two genes that belong to type III secretion system (TTSS), two hypothetical ORFS and, surprisingly, the <it>htrA </it>gene, a gene reported as involved with the virulence process in animal-pathogenic bacteria but not described as involved in phytobacteria virulence. Nucleic acid hybridization using labeled cDNA probes showed that some of the mutated genes are differentially expressed when the bacterium is grown in citrus leaves. Finally, comparative genomic analysis revealed that 5 mutated ORFs are in new putative pathogenicity islands.</p> <p>Conclusion</p> <p>The identification of these new genes related with Xcc infection and virulence is a great step towards the understanding of plant-pathogen interactions and could allow the development of strategies to control citrus canker.</p