164 research outputs found
Thermal expansion, heat capacity and magnetostriction of RAl (R = Tm, Yb, Lu) single crystals
We present thermal expansion and longitudinal magnetostriction data for cubic
RAl3 (R = Tm, Yb, Lu) single crystals. The thermal expansion coefficient for
YbAl3 is consistent with an intermediate valence of the Yb ion, whereas the
data for TmAl3 show crystal electric field contributions and have strong
magnetic field dependencies. de Haas-van Alphen-like oscillations were observed
in the magnetostriction data of YbAl3 and LuAl3, several new extreme orbits
were measured and their effective masses were estimated. Zero and 140 kOe
specific heat data taken on both LuAl3 and TmAl3 for T < 200 K allow for the
determination of a CEF splitting scheme for TmAl3
EFECTO DE PROTECT - ITĀ® PARA EL CONTROL DEL GORGOJO, SITOPHILUS ZEA MAIS EN MAĆZ ALMACENADO / EFFECT OF PROTECT - ITĀ® FOR THE CONTROL OF WEEVIL, SITOPHILUS ZEA MAIS IN STORED CORN
El gorgojo del MaĆz (Sitophilus zeamais (M) es considerada una de las plagas mĆ”s importantes que afectan el maĆz almacenado, por esto, el objetivo de la presente investigaciĆ³n fue determinar el efecto que ejerce la tierra de diatomea (Protect - ItĀ®) sobre el control de esta plaga. Los tratamientos evaluados fueron: Tierra de diatomea a dosis de 0.2, 0.5, 1.0, 2.0, y 3.0, g kg-1 de semilla, Actellic 50 CE a 0.5 mL por kg-1 de semilla y un testigo. Se usĆ³ un diseƱo completamente al azar con siete tratamientos y cuatro repeticiones y la variable de respuesta, porcentaje de mortalidad y germinaciĆ³n de semilla. La mortalidad de los insectos se determinĆ³ en cada unidad experimental con una frecuencia de 7, 14, 21, 30 dĆas despuĆ©s de la aplicaciĆ³n con tierra de diatomea (Protect - ItĀ®). Los resultados indican que el porcentaje de mortalidad promedio en las evaluaciones registradas a los 30 dĆas fue de 85, 98.7, 100 %; para las dosis de de 0.2, 0.5, 1.0, 2.0, y 3.0, g kg-1 de tierra de diatomea a los 7, 14, 21 y 30 dĆas respectivamente. La tierra de diatomea no afectĆ³ la germinaciĆ³n de maĆz cuando fueron tratadas con una dosis de 0.5 g kg-1 de semillas
PLAGAS TRANSFRONTERIZAS INTERCEPTADAS EN EL AEREOPUERTO JARDINES DEL REY / CROSS-BORDER PESTS INTERCEPTED IN JARDINES DEL REY AIRPORT
El presente trabajo se realizĆ³ en el punto de entrada del Aeropuerto Jardines del Rey, con el objetivo de determinar el ingreso de plagas transfronterizas desde el aƱo 2013 al 2017. Se decomisaron 3782,8 Kg de frutos, vegetales y semillas y en estos se realizaron 279 intercepciones. En los decomisos se observaron 124 muestras con huevos y adultos de Panonychus ulmis (Koch), 43 con Aonidiella aurantii, 37 Crysomphalum aonidum y Tetranychus tumidus Banks con 35. Se interceptĆ³ Tetranychus pacificus McGregor en fresa, procedente de CanadĆ”, con importancia cuarentenaria para nuestro paĆs y no hubo captura de Ceratitis capitata. Se sugiere un AnĆ”lisis de Riesgo para Plagas Cuarentenarias en los frutales y fortalecer el conocimiento de los inspectores de cuarentena en prediagnĆ³stico de Ćcaros e insectos como las moscas del gĆ©nero Ceratitis, Bactrocera y Anastrepha
Chronic Stress Induces Maladaptive Behaviors by Activating Corticotropin-Releasing Hormone Signaling in the Mouse Oval Bed Nucleus of the Stria Terminalis
The bed nucleus of the stria terminalis (BNST) is a forebrain region highly responsive to stress that expresses corticotropin-releasing hormone (CRH) and is implicated in mood disorders, such as anxiety. However, the exact mechanism by which chronic stress induces CRH-mediated dysfunction in BNST and maladaptive behaviors remains unclear. Here, we first confirmed that selective acute optogenetic activation of the oval nucleus BNST (ovBNST) increases maladaptive avoidance behaviors in male mice. Next, we found that a 6 week chronic variable mild stress (CVMS) paradigm resulted in maladaptive behaviors and increased cellular excitability of ovBNST CRH neurons by potentiating mEPSC amplitude, altering the resting membrane potential, and diminishing M-currents (a voltage-gated K+Ā current that stabilizes membrane potential) inĀ ex vivoĀ slices. CVMS also increased c-fos+Ā cells in ovBNST following handling. We next investigated potential molecular mechanism underlying the electrophysiological effects and observed that CVMS increased CRH+Ā and pituitary adenylate cyclase-activating polypeptide+Ā (PACAP; a CRH upstream regulator) cells but decreased striatal-enriched protein tyrosine phosphatase+Ā (a STEP CRH inhibitor) cells in ovBNST. Interestingly, the electrophysiological effects of CVMS were reversed by CRHR1-selective antagonist R121919 application. CVMS also activated protein kinase A (PKA) in BNST, and chronic infusion of the PKA-selective antagonist H89 into ovBNST reversed the effects of CVMS. Coadministration of the PKA agonist forskolin prevented the beneficial effects of R121919. Finally, CVMS induced an increase in surface expression of phosphorylated GluR1 (S845) in BNST. Collectively, these findings highlight a novel and indispensable stress-induced role for PKA-dependent CRHR1 signaling in activating BNST CRH neurons and mediating maladaptive behaviors
Exploiting protein flexibility to predict the location of allosteric sites
Background: Allostery is one of the most powerful and common ways of regulation of protein activity. However, for most allosteric proteins identified to date the mechanistic details of allosteric modulation are not yet well understood. Uncovering common mechanistic patterns underlying allostery would allow not only a better academic understanding of the phenomena, but it would also streamline the design of novel therapeutic solutions. This relatively unexplored therapeutic potential and the putative advantages of allosteric drugs over classical active-site inhibitors fuel the attention allosteric-drug research is receiving at present. A first step to harness the regulatory potential and versatility of allosteric sites, in the context of drug-discovery and design, would be to detect or predict their presence and location. In this article, we describe a simple computational approach, based on the effect allosteric ligands exert on protein flexibility upon binding, to predict the existence and position of allosteric sites on a given protein structure. Results: By querying the literature and a recently available database of allosteric sites, we gathered 213 allosteric proteins with structural information that we further filtered into a non-redundant set of 91 proteins. We performed normal-mode analysis and observed significant changes in protein flexibility upon allosteric-ligand binding in 70% of the cases. These results agree with the current view that allosteric mechanisms are in many cases governed by changes in protein dynamics caused by ligand binding. Furthermore, we implemented an approach that achieves 65% positive predictive value in identifying allosteric sites within the set of predicted cavities of a protein (stricter parameters set, 0.22 sensitivity), by combining the current analysis on dynamics with previous results on structural conservation of allosteric sites. We also analyzed four biological examples in detail, revealing that this simple coarse-grained methodology is able to capture the effects triggered by allosteric ligands already described in the literature. Conclusions: We introduce a simple computational approach to predict the presence and position of allosteric sites in a protein based on the analysis of changes in protein normal modes upon the binding of a coarse-grained ligand at predicted cavities. Its performance has been demonstrated using a newly curated non-redundant set of 91 proteins with reported allosteric properties. The software developed in this work is available upon request from the authors
Biomarker candidates of neurodegeneration in Parkinsonās disease for the evaluation of disease-modifying therapeutics
Reliable biomarkers that can be used for early diagnosis and tracking disease progression are the cornerstone of the development of disease-modifying treatments for Parkinsonās disease (PD). The German Society of Experimental and Clinical Neurotherapeutics (GESENT) has convened a Working Group to review the current status of proposed biomarkers of neurodegeneration according to the following criteria and to develop a consensus statement on biomarker candidates for evaluation of disease-modifying therapeutics in PD. The criteria proposed are that the biomarker should be linked to fundamental features of PD neuropathology and mechanisms underlying neurodegeneration in PD, should be correlated to disease progression assessed by clinical rating scales, should monitor the actual disease status, should be pre-clinically validated, and confirmed by at least two independent studies conducted by qualified investigators with the results published in peer-reviewed journals. To date, available data have not yet revealed one reliable biomarker to detect early neurodegeneration in PD and to detect and monitor effects of drug candidates on the disease process, but some promising biomarker candidates, such as antibodies against neuromelanin, pathological forms of Ī±-synuclein, DJ-1, and patterns of gene expression, metabolomic and protein profiling exist. Almost all of the biomarker candidates were not investigated in relation to effects of treatment, validated in experimental models of PD and confirmed in independent studies
Thiram inhibits angiogenesis and slows the development of experimental tumours in mice
Thiram-tetramethylthiuram disulphide ā a chelator of heavy metals, inhibited DNA synthesis and induced apoptosis in cultured bovine capillary endothelial cells. Bovine capillary endothelial cells were 10ā60-fold more sensitive to thiram than other cell types. These effects were prevented by addition of antioxidants, indicating involvement of reactive oxygen species. Exogenously added Cu2+ impeded specifically and almost completely the inhibitory effect of thiram for bovine capillary endothelial cells. Moreover, thiram had markedly inhibited human recombinant Cu/Zn superoxide dismutase enzymatic activity (85%) in vitro. Moreover, PC12-SOD cells with elevated Cu/Zn superoxide dismutase were less sensitive to thiram treatment than control cells. These data indicate that the effects of thiram are mediated by inhibition of Cu/Zn superoxide dismutase activity. Oral administration of thiram (13ā30āĪ¼g mouseā1), inhibited angiogenesis in CD1 nude mice. Tumour development is known to largely depend on angiogenesis. We found that oral administration of thiram (30āĪ¼g) to mice caused significant inhibition of C6 glioma tumour development (60%) and marked reduction (by 3ā5-fold) in metastatic growth of Lewis lung carcinoma. The data establish thiram as a potential inhibitor of angiogenesis and raise the possibility for its use as therapy in pathologies in which neovascularisation is involved, including neoplasia
Progresso genĆ©tico com a seleĆ§Ć£o recorrente recĆproca para hĆbridos interpopulacionais de milho
- ā¦