Soil, water and nutrient loss under conventional and organic vegetable production managed in small farms

Agricultural systems with conventional tillage and intensive use of agrochemicals, especially those on high slopes and with shallow soils, have the potential to release pollutants. This study aimed at evaluating the soil, water and nutrient lost via agricultural runoff in large plots (small catchments) under conventional and organic farming of vegetables as well as under forest (control) system in a Cambisol in the Campestre catchment. Samples of runoff were collected biweekly for one year through a Coshocton wheel. The soil and water losses from the conventional farming were 218 and 6 times higher, respectively, than forest. Under organic farming the soil and water losses were 12 and 4 times higher, respectively, than forest. However the soil losses (0.5 to 114 kg ha^(−1) year^(−1)) are considered low in agronomy but environmentally represent a potential source of surface water contamination by runoff associated pollutants. The concentrations and losses of all forms of phosphorus (P) were higher in the conventional system (9.5, 0.9 and 0.3 mg L^(−1) of total P for conventional, organic and forest systems, respectively), while the organic system had the highest concentrations and losses of soluble nitrogen (4.7, 38.6 and 0.4 mg L^(−1) of NO_3-N, respectively). The percentage of bioavailable P was proportionally higher in the organic system (91% of total P lost was as bioavailable P), indicating greater potential for pollution in the short term.

Loss of wobble uridine modification in tRNA anticodons interferes with TOR pathway signaling

Previous work in yeast has suggested that modification of tRNAs, in particular uridine bases in the anticodon wobble position (U34), is linked to TOR (target of rapamycin) signaling. Hence, U34 modification mutants were found to be hypersensitive to TOR inhibition by rapamycin. To study whether this involves inappropriate TOR signaling, we examined interaction between mutations in TOR pathway genes (tip41Δ, sap190Δ, ppm1Δ, rrd1Δ) and U34 modification defects (elp3Δ, kti12Δ, urm1Δ, ncs2Δ) and found the rapamycin hypersensitivity in the latter is epistatic to drug resistance of the former. Epistasis, however, is abolished in tandem with a gln3Δ deletion, which inactivates transcription factor Gln3 required for TOR-sensitive activation of NCR (nitrogen catabolite repression) genes. In line with nuclear import of Gln3 being under control of TOR and dephosphorylation by the Sit4 phosphatase, we identify novel TOR-sensitive sit4 mutations that confer rapamycin resistance and importantly, mislocalise Gln3 when TOR is inhibited. This is similar to gln3Δ cells, which abolish the rapamycin hypersensitivity of U34 modification mutants, and suggests TOR deregulation due to tRNA undermodification operates through Gln3. In line with this, loss of U34 modifications (elp3Δ, urm1Δ) enhances nuclear import of and NCR gene activation (MEP2, GAP1) by Gln3 when TOR activity is low. Strikingly, this stimulatory effect onto Gln3 is suppressed by overexpression of tRNAs that usually carry the U34 modifications. Collectively, our data suggest that proper TOR signaling requires intact tRNA modifications and that loss of U34 modifications impinges on the TORsensitive NCR branch via Gln3 misregulation.

Loss of Anticodon Wobble Uridine Modifications Affects tRNALys Function and Protein Levels in Saccharomyces cerevisiae

In eukaryotes, wobble uridines in the anticodons of tRNALysUUU, tRNAGluUUC and tRNAGlnUUG are modified to 5-methoxy-carbonyl-methyl-2-thio-uridine (mcm5s2U). While mutations in subunits of the Elongator complex (Elp1-Elp6), which disable mcm5 side chain formation, or removal of components of the thiolation pathway (Ncs2/Ncs6, Urm1, Uba4) are individually tolerated, the combination of both modification defects has been reported to have lethal effects on Saccharomyces cerevisiae. Contrary to such absolute requirement of mcm5s2U for viability, we demonstrate here that in the S. cerevisiae S288C-derived background, both pathways can be simultaneously inactivated, resulting in combined loss of tRNA anticodon modifications (mcm5U and s2U) without a lethal effect. However, an elp3 disruption strain displays synthetic sick interaction and synergistic temperature sensitivity when combined with either uba4 or urm1 mutations, suggesting major translational defects in the absence of mcm5s2U modifications. Consistent with this notion, we find cellular protein levels drastically decreased in an elp3uba4 double mutant and show that this effect as well as growth phenotypes can be partially rescued by excess of tRNALysUUU. These results may indicate a global translational or protein homeostasis defect in cells simultaneously lacking mcm5 and s2 wobble uridine modification that could account for growth impairment and mainly originates from tRNALysUUU hypomodification and malfunction.

Neuroticism, intelligence, and intra-individual variability in elementary cognitive tasks : Testing the mental noise hypothesis. 'Neuroticismo, inteligencia y variabilidad intra-individual en tareas cognitivas elementales : contraste de la hip??tesis del ruido neuronal'

Resumen tomado de la publicaci??n

"Refined mapping of a quantitative trait locus on chromosome 1 responsible for mouse embryonic death"

Recurrent spontaneous abortion (RSA) is defined as the loss of three or more consecutive pregnancies during the first trimester of embryonic intrauterine development. This kind of human infertility is frequent among the general population since it affects 1 to 5% of women. In half of the cases the etiology remains unelucidated. In the present study, we used interspecific recombinant congenic mouse strains (IRCS) in the aim to identify genes responsible for embryonic lethality. Applying a cartographic approach using a genotype/phenotype association, we identified a minimal QTL region, of about 6 Mb on chromosome 1, responsible for a high rate of embryonic death (,30%). Genetic analysis suggests that the observed phenotype is linked to uterine dysfunction. Transcriptomic analysis of the uterine tissue revealed a preferential deregulation of genes of this region compared to the rest of the genome. Some genes from the QTL region are associated with VEGF signaling, mTOR signaling and ubiquitine/proteasome-protein degradation pathways. This work may contribute to elucidate the molecular basis of a multifactorial and complex human disorder as RSA.

Preferential binding to elk-1 by sle-associated il10 risk allele upregulates il10 expression

Immunoregulatory cytokine interleukin-10 (IL-10) is elevated in sera from patients with systemic lupus erythematosus (SLE) correlating with disease activity. The established association of IL10 with SLE and other autoimmune diseases led us to fine map causal variant(s) and to explore underlying mechanisms. We assessed 19 tag SNPs, covering the IL10 gene cluster including IL19, IL20 and IL24, for association with SLE in 15,533 case and control subjects from four ancestries. The previously reported IL10 variant, rs3024505 located at 1 kb downstream of IL10, exhibited the strongest association signal and was confirmed for association with SLE in European American (EA) (P = 2.7×10−8, OR = 1.30), but not in non-EA ancestries. SNP imputation conducted in EA dataset identified three additional SLE-associated SNPs tagged by rs3024505 (rs3122605, rs3024493 and rs3024495 located at 9.2 kb upstream, intron 3 and 4 of IL10, respectively), and SLE-risk alleles of these SNPs were dose-dependently associated with elevated levels of IL10 mRNA in PBMCs and circulating IL-10 protein in SLE patients and controls. Using nuclear extracts of peripheral blood cells from SLE patients for electrophoretic mobility shift assays, we identified specific binding of transcription factor Elk-1 to oligodeoxynucleotides containing the risk (G) allele of rs3122605, suggesting rs3122605 as the most likely causal variant regulating IL10 expression. Elk-1 is known to be activated by phosphorylation and nuclear localization to induce transcription. Of interest, phosphorylated Elk-1 (p-Elk-1) detected only in nuclear extracts of SLE PBMCs appeared to increase with disease activity. Co-expression levels of p-Elk-1 and IL-10 were elevated in SLE T, B cells and monocytes, associated with increased disease activity in SLE B cells, and were best downregulated by ERK inhibitor. Taken together, our data suggest that preferential binding of activated Elk-1 to the IL10 rs3122605-G allele upregulates IL10 expression and confers increased risk for SLE in European Americans.

Refined mapping of a quantitative trait locus on chromosome 1 responsible for mouse embryonic death

Recurrent spontaneous abortion (RSA) is defined as the loss of three or more consecutive pregnancies during the first trimester of embryonic intrauterine development. This kind of human infertility is frequent among the general population since it affects 1 to 5% of women. In half of the cases the etiology remains unelucidated. In the present study, we used interspecific recombinant congenic mouse strains (IRCS) in the aim to identify genes responsible for embryonic lethality. Applying a cartographic approach using a genotype/phenotype association, we identified a minimal QTL region, of about 6 Mb on chromosome 1, responsible for a high rate of embryonic death (similar to 30%). Genetic analysis suggests that the observed phenotype is linked to uterine dysfunction. Transcriptomic analysis of the uterine tissue revealed a preferential deregulation of genes of this region compared to the rest of the genome. Some genes from the QTL region are associated with VEGF signaling, mTOR signaling and ubiquitine/proteasome-protein degradation pathways. This work may contribute to elucidate the molecular basis of a multifactorial and complex human disorder as RSA.

Enfermedad de Creutzfeldt-Jakob esporádica: estudio clínico, patológico y molecular de un caso

Generalidades. Las encefalopatías espongiformes transmisibles son enfermedades neurodegenerativas ocasionadas por la acumulación anormal de una variante mal plegada de la proteína priónica, lo cual induce la formación de conglomerados proteicos resistentes a la degradación. Además, son responsables de la disfunción sináptica, daño neuronal y de la sintomatología clásica acompañante. Esta proteína de membrana es codificada por el exón 2 del gen PRNP, ubicado en el brazo corto del cromosoma 20 y parece estar involucrada en la trasmisión sináptica, la transducción de señales, la actividad antioxidante de la superoxidodismutasa, neuroplasticidad y sobrevida celular. Un polimorfismo en el codón 129 se asocia con una susceptibilidad diferencial a la enfermedad Creutzfeldt-Jakob esporádica. Objetivo. Estudio clínico, patológico y molecular de un caso de una mujer de 58 años con diagnóstico de enfermedad de Creutzfeldt- Jakob esporádica. Métodos y resultados. Se presenta el caso de una mujer en quien aparece un trastorno depresivo del afecto con demencia progresiva y sintomatología general. Al final de la enfermedad, el cuadro progresó a un déficit neurológico focalizado en el área visual. La RMN mostró hiperintensidades inespecíficas córtico-subcorticales en el núcleo estriado; en el EEG se encontró pérdida de ritmos de fondo, patrón de descargas periódicas generalizadas y complejos trifásicos; en la biopsia cerebral postmorten se evidenció pérdida severa de la población neuronal en todas las capas, vacuolas en el neuropil, en el soma neuronal y en la glía. El análisis de secuencia del gen PRNP, a partir de extracción de DNA de sangre periférica, identificó homocigosis para metionina en el codón 129. La paciente fallece a los 3 meses del inicio de la sintomatología. Conclusión. Por epidemiología, curso clínico y exámenes paraclínicos se confirma el diagnóstico de enfermedad de Creutzfeldt- Jakob esporádica.La determinación del genotipo para los polimorfismos de riesgo se convierte en una herramienta útil para complementar por medios moleculares el diagnóstico y para profundizar la comprensión de la fisiopatología de la enfermedad de Creutzfeldt-Jakob, tanto para formas esporádicas como para la nueva variante.

Loss of nerve fiber layer in HIV positive patients and comparative patterns in a series of cases in Bucaramanga, Colombia

Objective: The objective of this study is to conduct a description of the features of optic neuropathy associated with Human Immunodeficiency Virus in relation to their possible incidence within our population, regarding that there is no data in our population in terms of frequency of this pathology (1,2). Methodology: Descriptive cross-sectional study of a clinical series of patients infected with human immunodeficiency virus, but AIDS, and the thickness of optic nerve´s layer of fibers studied with OCT technology (optical coherence tomography), patients were cited once captured. OCT was performed by the same observer, by taking 3 shots and picking the one with better reliability. Patients were given personally to the Ophthalmologic Foundation of Santander to conduct the review called OCT (optical coherence tomography). Results: In terms of viral load variable, we found a clear correlation in which validates the hypothesis that lower viral load means a thicker layer of fibers finding statistically significant differences for the 6 hours in right eye and 12 and 6 hours in left eye. Comparison between the known nomogram of fiber layer thickness for the population of Bucaramanga, Santander and thickness found in our sample, we note a clear decrease in the upper and lower quadrants, specifically in 7 hours and 11 hours, being more important in 7 hours, showing statistically significant differences. Conclusions: The pattern  of thinning of the nerve fiber layer in HIV positive patients without AIDS, and antiretroviral treatment type HAART, showed a statistically significant thinning targeted at 7 hours and 11 hours, being higher in first. Viral load figures have a direct relation with loss fiber layer, showing a statistically significant difference for the 6 and 12 hours.

Business cycle asymmetries: Loss aversion, sticky prices, and wages

In this chapter, the Smets-Wouters (2003) New Kenesian model is reformulated by introducing the loss aversion utility function developed in chapter two. The purpose of this is to understand how asymmetric real business cycles are linked to asymmetric behavior of agents in a price and wage rigidities set up. The simulations of the model reveal not only that the loss aversion in consumption and leisure is a good mechanism channel for explaining business cycle asymmetries, but also is a good mechanism channel for explaining asymmetric adjustment of prices and wages. Therefore the existence of asymmetries in Phillips Curve. Moreover, loss aversion makes downward rigidities in prices and wages stronger and also reproduces a more severe and persistent fall of the employment. All in all, this model generates asymmetrical real business cycles, asymmetric price and wage adjustment as well as hysteresis.

A DSGE model with loss aversion in consumption and leisure: an explanation for business cycles asymmetries

In this chapter, an asymmetric DSGE model is built in order to account for asymmetries in business cycles. One of the most important contributions of this work is the construction of a general utility function which nests loss aversion, risk aversion and habits formation by means of a smooth transition function. The main idea behind this asymmetric utility function is that under recession the agents over-smooth consumption and leisure choices in order to prevent a huge deviation of them from the reference level of the utility; while under boom, the agents simply smooth consumption and leisure, but trying to be as far as possible from the reference level of utility. The simulations of this model by means of Perturbations Method show that it is possible to reproduce asymmetrical business cycles where recession (on shock) are stronger than booms and booms are more long-lasting than recession. One additional and unexpected result is a downward stickiness displayed by real wages. As a consequence of this, there is a more persistent fall in employment in recession than in boom. Thus, the model reproduces not only asymmetrical business cycles but also real stickiness and hysteresis.

Escala de ajuste a la pérdida visual relacionada con la edad : adaptación española de la Age-related Vision Loss Scale (AVL Scale) de A. Horowitz y J. P. Reinhardt.

Resumen tomado de la publicación

Canonical syllable reduplication in infants with sensorineural hearing loss. 'Reduplicación y mezcla de sílabas balbuceadas en niños con hipoacusia'.

Resumen en español. Resumen basado en el de la publicación

El sujeto neuronal : aportaciones para una pedagogía de la posibilidad.

Resumen basado en el de la publicación

Viaje al universo neuronal : unidad did??ctica

Resumen basado en el de la publicaci??n