Movement between crops and weeds: temporal refuges for aphidophagous insects in Central Chile

Villegas, CM (Villegas, Cinthya M.)[ 1 ] ; Verdugo, JA (Verdugo, Jaime A.)[ 1,3 ] ; Tapia, J (Tapia, Jaime)[ 2 ] ; Lavandero, B (Lavandero, Bias)[ 1 ].1 ] Univ Talca, Inst Biol Vegetal & Biotecnol, Talca, Chile.2 ] Univ Talca, Inst Quim Recursos Nat, Talca, ChileCrop edges have significant effects on populations of natural enemies, acting as source or sink habitats during the growing season. Previous observations have shown that coccinellid species are associated with thistle (Sylibum marianum (L.) Gaertn), a common exotic weed in the central valley of Chile. To determine whether thistles growing at crop edges act as a putative refuge for natural enemies, the seasonal relative abundance of aphidophagous coccinellids was estimated at 0, 10 and 25 m from the edges of three alfalfa fields. Mark-recapture studies were carried out using the trace element rubidium (Rb) to determine whether coccinellids moved between the edges and the alfalfa. The most common aphidophagous coccinellid species were Hippodamia convergens (63%), H. variegata (11%), Rhyzobius lophantae (4%) and Adalia angulifera (4%). In mid-November, the abundance of coccinellids at the edge of (0 m from the edge) the alfalfa plot increased compared to that at the center of the field (25 m from the edge), coinciding with a reduction in the population of aphids at all sampling points. Of the coccinellids captured at the thistle edge, 68% were marked with rubidium, suggesting movement of coccinellids from the alfalfa plot to the thistle growing at its edges. After the thistles were removed, coccinellids returned to the crop, as shown by the presence of marked coccinellids within the alfalfa fields at all three sampling distances. The results of this study suggest that thistles can act as a refuge for coccinellids when aphids are not available in the alfalfa fields

Aumentar la biodiversidad en predios chilenos requiere de protocolos agroecológicos adaptados localmente

In the 1992 Earth Summit held in Rio de Janeiro, Brazil, the concept of sustainable development, un­derstood as the balance between economic, social, and environmental factors interacting in space and time, was recognized by representatives from 179 countries as vital to sustain human life without compromising the planet (United Nations, 1992). Nowadays, as hu­manity faces unseen anthropogenic problems such as climate change and biodiversity loss (IPCC, 2021), the concept of sustainable development has been recently highlighted by United Nations through the creation of 17 Sustainable Development Goals, aiming at impro­ving environmental and human well-being globally (United Nations, 2015).In the 1992 Earth Summit held in Rio de Janeiro, Brazil, the concept of sustainable development, un­derstood as the balance between economic, social, and environmental factors interacting in space and time, was recognized by representatives from 179 countries as vital to sustain human life without compromising the planet (United Nations, 1992). Nowadays, as hu­manity faces unseen anthropogenic problems such as climate change and biodiversity loss (IPCC, 2021), the concept of sustainable development has been recently highlighted by United Nations through the creation of 17 Sustainable Development Goals, aiming at impro­ving environmental and human well-being globally (United Nations, 2015)

Measurement of the Bottom-Strange Meson Mixing Phase in the Full CDF Data Set

We report a measurement of the bottom-strange meson mixing phase \beta_s using the time evolution of B0_s -> J/\psi (->\mu+\mu-) \phi (-> K+ K-) decays in which the quark-flavor content of the bottom-strange meson is identified at production. This measurement uses the full data set of proton-antiproton collisions at sqrt(s)= 1.96 TeV collected by the Collider Detector experiment at the Fermilab Tevatron, corresponding to 9.6 fb-1 of integrated luminosity. We report confidence regions in the two-dimensional space of \beta_s and the B0_s decay-width difference \Delta\Gamma_s, and measure \beta_s in [-\pi/2, -1.51] U [-0.06, 0.30] U [1.26, \pi/2] at the 68% confidence level, in agreement with the standard model expectation. Assuming the standard model value of \beta_s, we also determine \Delta\Gamma_s = 0.068 +- 0.026 (stat) +- 0.009 (syst) ps-1 and the mean B0_s lifetime, \tau_s = 1.528 +- 0.019 (stat) +- 0.009 (syst) ps, which are consistent and competitive with determinations by other experiments.Comment: 8 pages, 2 figures, Phys. Rev. Lett 109, 171802 (2012

Testosterone activates glucose metabolism through AMPK and androgen signaling in cardiomyocyte hypertrophy

Background: Testosterone regulates nutrient and energy balance to maintain protein synthesis and metabolism in cardiomyocytes, but supraphysiological concentrations induce cardiac hypertrophy. Previously, we determined that testosterone increased glucose uptake—via AMP-activated protein kinase (AMPK)—after acute treatment in cardiomyocytes. However, whether elevated glucose uptake is involved in long-term changes of glucose metabolism or is required during cardiomyocyte growth remained unknown. In this study, we hypothesized that glucose uptake and glycolysis increase in testosterone-treated cardiomyocytes through AMPK and androgen receptor (AR). Methods: Cultured cardiomyocytes were stimulated with 100 nM testosterone for 24 h, and hypertrophy was verified by increased cell size and mRNA levels of β-myosin heavy chain (β-mhc). Glucose uptake was assessed by 2-NBDG. Glycolysis and glycolytic capacity were determined by measuring extracellular acidification rate (ECAR). Results: Testosterone induced cardiomyocyte hypertrophy that was accompanied by increased glucose uptake, glycolysis enhancement and upregulated mRNA expression of hexokinase 2. In addition, testosterone increased AMPK phosphorylation (Thr172), while inhibition of both AMPK and AR blocked glycolysis and cardiomyocyte hypertrophy induced by testosterone. Moreover, testosterone supplementation in adult male rats by 5 weeks induced cardiac hypertrophy and upregulated β-mhc, Hk2 and Pfk2 mRNA levels. Conclusion: These results indicate that testosterone stimulates glucose metabolism by activation of AMPK and AR signaling which are critical to induce cardiomyocyte hypertrophy.Fil: Troncoso, Mayarling Francisca. Universidad de Chile; ChileFil: Pavez, Mario. Universidad de Chile; ChileFil: Wilson Rodriguez, Carlos. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra. Universidad Nacional de Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra; Argentina. Universidad de Chile; ChileFil: Lagos, Daniel. Universidad de Chile; ChileFil: Duran, Javier. Universidad de Chile; ChileFil: Ramos, Sebastián. Universidad de Chile; ChileFil: Barrientos, Genaro. Universidad de Chile; ChileFil: Silva, Patricio. Universidad Central de Chile; ChileFil: Llanos, Paola. Universidad de Chile; ChileFil: Basualto Alarcón, Carla. Universidad de Chile; Chile. Universidad de Aysén; ChileFil: Westenbrink, B. Daan. University of Groningen; Países BajosFil: Lavandero, Sergio. Universidad de Chile; Chile. Texas A&M University; Estados UnidosFil: Estrada, Manuel. Universidad de Chile; Chil

The complex interplay between mitochondrial dynamics and cardiac metabolism

Artículo de publicación ISIMitochondria are highly dynamic organelles, capable of undergoing constant fission and fusion events, forming networks. These dynamic events allow the transmission of chemical and physical messengers and the exchange of metabolites within the cell. In this article we review the signaling mechanisms controlling mitochondrial fission and fusion, and its relationship with cell bioenergetics, especially in the heart. Furthermore we also discuss how defects in mitochondrial dynamics might be involved in the pathogenesis of metabolic cardiac diseases

Neutral endopeptidase and angiotensin I converting enzyme insertion/deletion gene polymorphism in humans

Neutral endopeptidase (NEP) hydrolyses angiotensins (Ang) I and II and generates angiotensin-(1-7) [Ang-(17)]. In humans, the insertion/deletion (I/D) angiotensin- I converting enzyme ( ACE) gene polymorphism determined plasma ACE levels by 40%. In rats, a similar polymorphism determines ACE levels which are inversely associated to NEP activity. The objective of this study is to evaluate the relationship between ACE expression and plasma NEP activity in normotensive subjects and in hypertensive patients. In total, 58 consecutive patients with hypertension, evaluated in our Hypertension Clinic, were compared according to their ACE I/D genotypes with 54 control subjects in terms of both plasma ACE activity and NEP activities. Plasma ACE activity was elevated 51 and 70% in both DD ACE groups ( normotensives and hypertensives) compared with their respective ID and II ACE groups ( P<0.001). A significant effect of the ACE polymorphism and of the hypertensive status on ACE activity was observed (P<0.001). In normotensive DD ACE subjects, NEP activity was 0.30 +/- 0.02 U/ml, whereas in the normotensive II ACE and in the normotensive ID ACE subjects NEP activity was increased 65 and 48%, respectively ( P<0.001). In the hypertensive DD ACE patients, NEP activity was 0.47 +/- 0.03 U/mg. An effect of the I/D ACE genotypes on NEP activity (P<0.04) and an interaction effect between the I/D ACE genotype and the hypertensive status were also observed (P<0.001). These results are consistent with a normal and inverse relationship between the ACE polymorphism and NEP activity in normotensive humans ( as is also observed in rats). This normal relationship is not observed in hypertensive patients

NFAT5 Is Activated by Hypoxia: Role in Ischemia and Reperfusion in the Rat Kidney

The current hypothesis postulates that NFAT5 activation in the kidney's inner medulla is due to hypertonicity, resulting in cell protection. Additionally, the renal medulla is hypoxic (10–18 mmHg); however there is no information about the effect of hypoxia on NFAT5. Using in vivo and in vitro models, we evaluated the effect of reducing the partial pressure of oxygen (PO2) on NFAT5 activity. We found that 1) Anoxia increased NFAT5 expression and nuclear translocation in primary cultures of IMCD cells from rat kidney. 2) Anoxia increased transcriptional activity and nuclear translocation of NFAT5 in HEK293 cells. 3) The dose-response curve demonstrated that HIF-1α peaked at 2.5% and NFAT5 at 1% of O2. 4) At 2.5% of O2, the time-course curve of hypoxia demonstrated earlier induction of HIF-1α gene expression than NFAT5. 5) siRNA knockdown of NFAT5 increased the hypoxia-induced cell death. 6) siRNA knockdown of HIF-1α did not affect the NFAT5 induction by hypoxia. Additionally, HIF-1α was still induced by hypoxia even when NFAT5 was knocked down. 7) NFAT5 and HIF-1α expression were increased in kidney (cortex and medulla) from rats subjected to an experimental model of ischemia and reperfusion (I/R). 7) Experimental I/R increased the NFAT5-target gene aldose reductase (AR). 8) NFAT5 activators (ATM and PI3K) were induced in vitro (HEK293 cells) and in vivo (I/R kidneys) with the same timing of NFAT5. 8) Wortmannin, which inhibits ATM and PI3K, reduces hypoxia-induced NFAT5 transcriptional activation in HEK293 cells. These results demonstrate for the first time that NFAT5 is induced by hypoxia and could be a protective factor against ischemic damage

A BAX/BAK and Cyclophilin D-Independent Intrinsic Apoptosis Pathway

Most intrinsic death signals converge into the activation of pro-apoptotic BCL-2 family members BAX and BAK at the mitochondria, resulting in the release of cytochrome c and apoptosome activation. Chronic endoplasmic reticulum (ER) stress leads to apoptosis through the upregulation of a subset of pro-apoptotic BH3-only proteins, activating BAX and BAK at the mitochondria. Here we provide evidence indicating that the full resistance of BAX and BAK double deficient (DKO) cells to ER stress is reverted by stimulation in combination with mild serum withdrawal. Cell death under these conditions was characterized by the appearance of classical apoptosis markers, caspase-9 activation, release of cytochrome c, and was inhibited by knocking down caspase-9, but insensitive to BCL-XL overexpression. Similarly, the resistance of BIM and PUMA double deficient cells to ER stress was reverted by mild serum withdrawal. Surprisingly, BAX/BAK-independent cell death did not require Cyclophilin D (CypD) expression, an important regulator of the mitochondrial permeability transition pore. Our results suggest the existence of an alternative intrinsic apoptosis pathway emerging from a cross talk between the ER and the mitochondria

Crop pests and predators exhibit inconsistent responses to surrounding landscape composition

The idea that noncrop habitat enhances pest control and represents a win–win opportunity to conserve biodiversity and bolster yields has emerged as an agroecological paradigm. However, while noncrop habitat in landscapes surrounding farms sometimes benefits pest predators, natural enemy responses remain heterogeneous across studies and effects on pests are inconclusive. The observed heterogeneity in species responses to noncrop habitat may be biological in origin or could result from variation in how habitat and biocontrol are measured. Here, we use a pest-control database encompassing 132 studies and 6,759 sites worldwide to model natural enemy and pest abundances, predation rates, and crop damage as a function of landscape composition. Our results showed that although landscape composition explained significant variation within studies, pest and enemy abundances, predation rates, crop damage, and yields each exhibited different responses across studies, sometimes increasing and sometimes decreasing in landscapes with more noncrop habitat but overall showing no consistent trend. Thus, models that used landscape-composition variables to predict pest-control dynamics demonstrated little potential to explain variation across studies, though prediction did improve when comparing studies with similar crop and landscape features. Overall, our work shows that surrounding noncrop habitat does not consistently improve pest management, meaning habitat conservation may bolster production in some systems and depress yields in others. Future efforts to develop tools that inform farmers when habitat conservation truly represents a win–win would benefit from increased understanding of how landscape effects are modulated by local farm management and the biology of pests and their enemies

Increased ER-mitochondrial coupling promotes mitochondrial respiration and bioenergetics during early phases of ER stress

Artículo de publicación ISIIncreasing evidence indicates that endoplasmic reticulum (ER) stress activates the adaptive unfolded protein response (UPR), but that beyond a certain degree of ER damage, this response triggers apoptotic pathways. The general mechanisms of the UPR and its apoptotic pathways are well characterized. However, the metabolic events that occur during the adaptive phase of ER stress, before the cell death response, remain unknown. Here, we show that, during the onset of ER stress, the reticular and mitochondrial networks are redistributed towards the perinuclear area and their points of connection are increased in a microtubule-dependent fashion. A localized increase in mitochondrial transmembrane potential is observed only in redistributed mitochondria, whereas mitochondria that remain in other subcellular zones display no significant changes. Spatial re-organization of these organelles correlates with an increase in ATP levels, oxygen consumption, reductive power and increased mitochondrial Ca(2+) uptake. Accordingly, uncoupling of the organelles or blocking Ca(2+) transfer impaired the metabolic response, rendering cells more vulnerable to ER stress. Overall, these data indicate that ER stress induces an early increase in mitochondrial metabolism that depends crucially upon organelle coupling and Ca(2+) transfer, which, by enhancing cellular bioenergetics, establishes the metabolic basis for the adaptation to this response