Yield reductions in grain maize associated with the presence of European corn borer and Gibberella stalk rot in Québec

L'effet d'une infestation de la pyrale du maïs (Ostrinia nubilalis) [Lepidoptera: Pyralidae] et d'une infection de la fusariose des tiges causée par Gibberella zeae sur le rendement de huit lignées de maïs grain (Zea mays), de deux hybrides commerciaux et de six hybrides expérimentaux a été évalué de 1975 à 1980. Trois critères ont été utilisés: la criblure du feuillage, les dégâts totaux des plantes à la récolte et le rapport de la longueur des galeries creusées par les chenilles de pyrale dans les tiges sur la hauteur totale du plant. Pour la plupart des critères, les cultivars étaient significativement différents et l'infestation artificielle de pyrale du maïs a eu un effet presqu'à chaque année. Bien que le G. zeae ait eu un effet significatif sur les dégâts totaux à la récolte et le rendement en grain du maïs, aucune relation n'a pu être établie entre la maladie et la pyrale du maïs.The impact of European corn borer (Ostrinia nubilalis) [Lepidoptera: Pyralidae] infestation and stalk rot infection caused by Gibberella zeae on yield of eight grain maize (Zea mays) inbreds, two commercial and six experimental hybrids was evaluated from 1975 to 1980. Three criteria were used: leaf feeding, total plant damage at harvest and tunnel length/plant height ratio. For most criteria, the cultivars were significantly different and the artificial European corn borer infestation had an effect almost every year. Although G. zeae can have a signifiant effect on plant damage at harvest and yield of grain maize, no consistent link was found between stalk rot and European corn borer

Soliton pinning by long-range order in aperiodic systems

We investigate propagation of a kink soliton along inhomogeneous chains with two different constituents, arranged either periodically, aperiodically, or randomly. For the discrete sine-Gordon equation and the Fibonacci and Thue-Morse chains taken as examples, we have found that the phenomenology of aperiodic systems is very peculiar: On the one hand, they exhibit soliton pinning as in the random chain, although the depinning forces are clearly smaller. In addition, solitons are seen to propagate differently in the aperiodic chains than on periodic chains with large unit cells, given by approximations to the full aperiodic sequence. We show that most of these phenomena can be understood by means of simple collective coordinate arguments, with the exception of long range order effects. In the conclusion we comment on the interesting implications that our work could bring about in the field of solitons in molecular (e.g., DNA) chains.Comment: 4 pages, REVTeX 3.0 + epsf, 3 figures in accompanying PostScript file (Submitted to Phys Rev E Rapid Comm

Anomalous acoustic reflection on a sliding interface or a shear band

We study the reflection of an acoustic plane wave from a steadily sliding planar interface with velocity strengthening friction or a shear band in a confined granular medium. The corresponding acoustic impedance is utterly different from that of the static interface. In particular, the system being open, the energy of an in-plane polarized wave is no longer conserved, the work of the external pulling force being partitioned between frictional dissipation and gain (of either sign) of coherent acoustic energy. Large values of the friction coefficient favor energy gain, while velocity strengthening tends to suppress it. An interface with infinite elastic contrast (one rigid medium) and V-independent (Coulomb) friction exhibits spontaneous acoustic emission, as already shown by M. Nosonovsky and G.G. Adams (Int. J. Ing. Sci., {\bf 39}, 1257 (2001)). But this pathology is cured by any finite elastic contrast, or by a moderately large V-strengthening of friction. We show that (i) positive gain should be observable for rough-on-flat multicontact interfaces (ii) a sliding shear band in a granular medium should give rise to sizeable reflection, which opens a promising possibility for the detection of shear localization.Comment: 13 pages, 10 figure

The Therapeutic effect of Memantine through the Stimulation of Synapse Formation and Dendritic Spine Maturation in Autism and Fragile X Syndrome

Although the pathogenic mechanisms that underlie autism are not well understood, there is evidence showing that metabotropic and ionotropic glutamate receptors are hyper-stimulated and the GABAergic system is hypo-stimulated in autism. Memantine is an uncompetitive antagonist of NMDA receptors and is widely prescribed for treatment of Alzheimer's disease treatment. Recently, it has been shown to improve language function, social behavior, and self-stimulatory behaviors of some autistic subjects. However the mechanism by which memantine exerts its effect remains to be elucidated. In this study, we used cultured cerebellar granule cells (CGCs) from Fmr1 knockout (KO) mice, a mouse model for fragile X syndrome (FXS) and syndromic autism, to examine the effects of memantine on dendritic spine development and synapse formation. Our results show that the maturation of dendritic spines is delayed in Fmr1-KO CGCs. We also detected reduced excitatory synapse formation in Fmr1-KO CGCs. Memantine treatment of Fmr1-KO CGCs promoted cell adhesion properties. Memantine also stimulated the development of mushroom-shaped mature dendritic spines and restored dendritic spine to normal levels in Fmr1-KO CGCs. Furthermore, we demonstrated that memantine treatment promoted synapse formation and restored the excitatory synapses to a normal range in Fmr1-KO CGCs. These findings suggest that memantine may exert its therapeutic capacity through a stimulatory effect on dendritic spine maturation and excitatory synapse formation, as well as promoting adhesion of CGCs

Reflexiones universitarias. San Pedro Valencia: renovación urbana, saneamiento ambiental y emprendimientos turísticos. Otoño 2015

Los trabajos que aquí se presentan se elaboraron por las y los estudiantes como parte de las actividades del Proyecto de Aplicación Profesional (PAP) “San Pedro Valencia: renovación urbana, saneamiento ambiental y emprendimientos turísticos”, durante el periodo de Otoño de 2015. A lo largo del periodo los autores compartieron sus reflexiones en torno a su percepción sobre el contexto en el que actúa el PAP; sobre las alternativas posibles a la problemática detectada y lo que significa pensar una alternativa; sobre los sujetos con los que se ha interactuado a lo largo de la experiencia de trabajo y sobre el papel del profesionista y del ciudadano en un mundo como el que nos tocó vivir. La obra está compuesta por reflexiones personales de las y los estudiantes que, explorando estas temáticas, comparten sus aprendizajes y observaciones de forma vívida.ITESO, A.C

A Study of Nuclear Transcription Factor-Kappa B in Childhood Autism

BACKGROUND: Several children with autism show regression in language and social development while maintaining normal motor milestones. A clear period of normal development followed by regression and subsequent improvement with treatment, suggests a multifactorial etiology. The role of inflammation in autism is now a major area of study. Viral and bacterial infections, hypoxia, or medication could affect both foetus and infant. These stressors could upregulate transcription factors like nuclear factor kappa B (NF-κB), a master switch for many genes including some implicated in autism like tumor necrosis factor (TNF). On this hypothesis, it was proposed to determine NF-κB in children with autism. METHODS: Peripheral blood samples of 67 children with autism and 29 control children were evaluated for NF-κB using electrophoretic mobility shift assay (EMSA). A phosphor imaging technique was used to quantify values. The fold increase over the control sample was calculated and statistical analysis was carried out using SPSS 15. RESULTS: We have noted significant increase in NF-κB DNA binding activity in peripheral blood samples of children with autism. When the fold increase of NF-κB in cases (n = 67) was compared with that of controls (n = 29), there was a significant difference (3.14 vs. 1.40, respectively; p<0.02). CONCLUSION: This finding has immense value in understanding many of the known biochemical changes reported in autism. As NF-κB is a response to stressors of several kinds and a master switch for many genes, autism may then arise at least in part from an NF-κB pathway gone awry

Disease-associated missense mutations in GluN2B subunit alter NMDA receptor ligand binding and ion channel properties.

Genetic and bioinformatic analyses have identified missense mutations in GRIN2B encoding the NMDA receptor GluN2B subunit in autism, intellectual disability, Lennox Gastaut and West Syndromes. Here, we investigated several such mutations using a near-complete, hybrid 3D model of the human NMDAR and studied their consequences with kinetic modelling and electrophysiology. The mutants revealed reductions in glutamate potency; increased receptor desensitisation; and ablation of voltage-dependent Mg block. In addition, we provide new views on Mg and NMDA channel blocker binding sites. We demonstrate that these mutants have significant impact on excitatory transmission in developing neurons, revealing profound changes that could underlie their associated neurological disorders. Of note, the NMDAR channel mutant GluN2B unusually allowed Mg permeation, whereas nearby N615I reduced Ca permeability. By identifying the binding site for an NMDAR antagonist that is used in the clinic to rescue gain-of-function phenotypes, we show that drug binding may be modified by some GluN2B disease-causing mutations

Rare mutations in N-methyl-D-aspartate glutamate receptors in autism spectrum disorders and schizophrenia

Pharmacological, genetic and expression studies implicate N-methyl-D-aspartate (NMDA) receptor hypofunction in schizophrenia (SCZ). Similarly, several lines of evidence suggest that autism spectrum disorders (ASD) could be due to an imbalance between excitatory and inhibitory neurotransmission. As part of a project aimed at exploring rare and/or de novo mutations in neurodevelopmental disorders, we have sequenced the seven genes encoding for NMDA receptor subunits (NMDARs) in a large cohort of individuals affected with SCZ or ASD (n=429 and 428, respectively), parents of these subjects and controls (n=568). Here, we identified two de novo mutations in patients with sporadic SCZ in GRIN2A and one de novo mutation in GRIN2B in a patient with ASD. Truncating mutations in GRIN2C, GRIN3A and GRIN3B were identified in both subjects and controls, but no truncating mutations were found in the GRIN1, GRIN2A, GRIN2B and GRIN2D genes, both in patients and controls, suggesting that these subunits are critical for neurodevelopment. The present results support the hypothesis that rare de novo mutations in GRIN2A or GRIN2B can be associated with cases of sporadic SCZ or ASD, just as it has recently been described for the related neurodevelopmental disease intellectual disability. The influence of genetic variants appears different, depending on NMDAR subunits. Functional compensation could occur to counteract the loss of one allele in GRIN2C and GRIN3 family genes, whereas GRIN1, GRIN2A, GRIN2B and GRIN2D appear instrumental to normal brain development and function

Hyperbaric treatment for children with autism: a multicenter, randomized, double-blind, controlled trial

<p>Abstract</p> <p>Background</p> <p>Several uncontrolled studies of hyperbaric treatment in children with autism have reported clinical improvements; however, this treatment has not been evaluated to date with a controlled study. We performed a multicenter, randomized, double-blind, controlled trial to assess the efficacy of hyperbaric treatment in children with autism.</p> <p>Methods</p> <p>62 children with autism recruited from 6 centers, ages 2–7 years (mean 4.92 ± 1.21), were randomly assigned to 40 hourly treatments of either hyperbaric treatment at 1.3 atmosphere (atm) and 24% oxygen ("treatment group", n = 33) or slightly pressurized room air at 1.03 atm and 21% oxygen ("control group", n = 29). Outcome measures included Clinical Global Impression (CGI) scale, Aberrant Behavior Checklist (ABC), and Autism Treatment Evaluation Checklist (ATEC).</p> <p>Results</p> <p>After 40 sessions, mean physician CGI scores significantly improved in the treatment group compared to controls in overall functioning (p = 0.0008), receptive language (p < 0.0001), social interaction (p = 0.0473), and eye contact (p = 0.0102); 9/30 children (30%) in the treatment group were rated as "very much improved" or "much improved" compared to 2/26 (8%) of controls (p = 0.0471); 24/30 (80%) in the treatment group improved compared to 10/26 (38%) of controls (p = 0.0024). Mean parental CGI scores significantly improved in the treatment group compared to controls in overall functioning (p = 0.0336), receptive language (p = 0.0168), and eye contact (p = 0.0322). On the ABC, significant improvements were observed in the treatment group in total score, irritability, stereotypy, hyperactivity, and speech (p < 0.03 for each), but not in the control group. In the treatment group compared to the control group, mean changes on the ABC total score and subscales were similar except a greater number of children improved in irritability (p = 0.0311). On the ATEC, sensory/cognitive awareness significantly improved (p = 0.0367) in the treatment group compared to the control group. Post-hoc analysis indicated that children over age 5 and children with lower initial autism severity had the most robust improvements. Hyperbaric treatment was safe and well-tolerated.</p> <p>Conclusion</p> <p>Children with autism who received hyperbaric treatment at 1.3 atm and 24% oxygen for 40 hourly sessions had significant improvements in overall functioning, receptive language, social interaction, eye contact, and sensory/cognitive awareness compared to children who received slightly pressurized room air.</p> <p>Trial Registration</p> <p>clinicaltrials.gov NCT00335790</p

Novel metabolic biomarkers related to sulfur-dependent detoxification pathways in autistic patients of Saudi Arabia

<p>Abstract</p> <p>Background</p> <p>Xenobiotics are neurotoxins that dramatically alter the health of the child. In addition, an inefficient detoxification system leads to oxidative stress, gut dysbiosis, and immune dysfunction. The consensus among physicians who treat autism with a biomedical approach is that those on the spectrum are burdened with oxidative stress and immune problems. In a trial to understand the role of detoxification in the etiology of autism, selected parameters related to sulfur-dependent detoxification mechanisms in plasma of autistic children from Saudi Arabia will be investigated compared to control subjects.</p> <p>Methods</p> <p>20 males autistic children aged 3-15 years and 20 age and gender matching healthy children as control group were included in this study. Levels of reduced glutathione (GSH), total (GSH+GSSG), glutathione status (GSH/GSSG), glutathione reductase (GR), glutathione- s-transferase (GST), thioredoxin (Trx), thioredoxin reductase (TrxR) and peroxidoxins (Prxs I and III) were determined.</p> <p>Results</p> <p>Reduced glutathione, total glutathione, GSH/GSSG and activity levels of GST were significantly lower, GR shows non-significant differences, while, Trx, TrxR and both Prx I and III recorded a remarkably higher values in autistics compared to control subjects.</p> <p>Conclusion</p> <p>The impaired glutathione status together with the elevated Trx and TrxR and the remarkable over expression of both Prx I and Prx III, could be used as diagnostic biomarkers of autism.</p