Efficacité Du Kaolin (Kalaba) Dans La Gestion Intégrée Des Chenilles Endocarpiques Du Cotonnier Dans La Zone Centre Du Bénin

The study on the efficacy of Kaolin in the integrated management of the endocarpiques larvae of cotton was undertaken in the center of Benin. The objective of the work was to evaluate the potentiality of Kaolin in the control of some endocarpiques larvae of the cotton plant. To achieve this goal, a Fisher block device with 4 treatments and 4 repetitions were set up on two sites. The treatments developed consisted of an untreated plot ; a plot treated with Lambdacyalothrine 15 g/l - chlorpyrifos ethyl 300 g/l; a plot treated with kaolin 5% and another one with the mixture kaolin + Lambdacyalothrine 15 g/l - chlorpyrifos ethyl 300 g/l. The treatment with kaolin was achieved with a back, maintained pressure sprayer. Ten applications were conducted with the kaolin used alone and 6 with the other objects. Results showed that there is no significant difference between the average number of larvae recorded in the plots treated with kaolin and plots which served as control of reference (Lambdacyalothrine 15 g/l - chlorpyrifos ethyl 300 g/l at 1 l/ha). It was the same for the percentage of attacked green capsules and cotton seed production. The effect of kaolin in the control of Haritalodes derogata was low (11.6% of plants attacked against 0.1 % for the chemical reference control and 22.9 % for the untreated plot). The results of Kaolin associated with the binary acaricide, showed that the number of endocarpiques larvae has been significantly reduced compared to the reference control. This study indicates that kaolin can be used like other biological pesticides, as alternative to chemical control and then, constituted an important component of the integrated cotton pests management

Le profenofos, un alternatif à l’endosulfan en culture cotonnière au Bénin

Dans l’objectif de trouver un alternatif à l’endosulfan, l’efficacité du profenofos et de l’endosulfan a été étudié dans un dispositif de bloc aléatoire complet en station et en milieu réel. Sur station, le profenofos assure un contrôle, équivalent et parfois significativement supérieur (p < 0,001) à l’endosulfan, des populations des ravageurs comme Helicoverpa armigera, Earias spp, Pectinophora gossypiella, Cryptophlebia leucotreta. Le Fanga 500 EC (profenofos 750 g/ha) a été significativement supérieur (p < 0,05) à Callisulfan 350 EC (endosulfan 700 g/ha) pour le contrôle des populations de Aphis gossypii, Pectinophora gossypiella et Earias spp. Il en résulte une production de capsules vertes saines qui montre que le Calfos 500 EC (profenofos 750 g/ha) est équivalent aux différentes formulations d’endosulfan testées et parfois significativement meilleur (p < 0,01) au Thiofanex 350 EC (endosulfan 700 g/ha). A la récolte du coton graine, le profenofos procure un rendement significativement supérieur (p < 0,05) à l’endosulfan. En milieu paysan, aucune différence significative (p > 0,05) n’a été observée entre le Calfos 500 EC (profenofos 750 g/ha) et le Callisulfan 350 EC (endosulfan 700 g/ha) à la récolte du coton graine. Le profenofos peut être appliqué comme un alternatif à l’endosulfan en culture cotonnière au Bénin.© 2016 International Formulae Group. All rights reserved.Mots clés: Profenofos, alternatif à l’endosulfan, culture cotonnière, BéninEnglish Title: The profenofos, an alternative to endosulfan in cotton crop in BeninEnglish AbstractIn the objective to find an alternative to endosulfan, the efficacy of profenofos and endosulfan has been studied in a complete randomized block design in experimentation station and in real environment. In station, the profenofos provides, in comparison with endosulfan, an equivalent control, and sometimes, a significantly higher (p < 0.001) control, of cotton pest populations including Helicoverpa armigera, Earias spp, Pectinophora gossypiella, Cryptophlebia leucotreta. The effect of Fanga 500 EC (profenofos 750 g/ha) has been significantly higher (p < 0.05) than the effect of Callisulfan 350 EC (endosulfan 700 g/ha) for the control of the populations of Aphis gossypii, Pectinophora gossypiella and Earias spp. It results, of this fact, a production of the best quality of cotton which shows that the Calfos 500 EC (profenofos 750 g/ha) is equivalent to various formulations of endosulfan tested and sometimes significantly better (p < 0.01) than Thiofanex 350 EC (endosulfan 700 g/ha). At harvest time, the profenofos provides a yield of seed cotton significantly higher (p < 0.05) than those obtained with endosulfan. In real environment, at harvest time of seed cotton, no  significant difference (p > 0.05) has been observed between the Calfos 500 EC (profenofos 750 g/ha) and the Callisulfan 350 EC (endosulfan 700 g/ha). The profenofos can be used as an alternative to endosulfan in cotton crop in Benin.© 2016 International Formulae Group. All rights reserved.Keywords: Profenofos, alternative to endosulfan, cotton crop, Beni

Depolarization-initiated endogenous cannabinoid release and underlying retrograde neurotransmission in interneurons of amygdala

The depolarization is also important for the short-term synaptic plasticity, known as depolarization-induced suppression of excitation (DSE). The two major types of neurons and their synapses in the lateral nucleus of amygdala (LA) are prone to plasticity. However, DSE in interneurons has not been reported in amygdala in general and in LA in particular. Therefore, we conducted the patch-clamp experiments with LA interneurons. These neurons were identified by lack of adaptation in firing rate of action potentials. In this study, we show for the first time a transient suppression of neurotransmission at synapses both within the local network and between cortical inputs and interneurons of the LA. The retrograde neurotransmission from GABAergic interneurons were comparable with that of glutamatergic pyramidal cells. That is the axonal terminals of cortical inputs do not posses selectivity toward two neuronal subtypes. However, the DSE of both types of neurons involve an increase in intracellular Ca[superscript 2+] and the release of endogenous cannabinoids (eCB) and activation of presynaptic CB1 receptors. The magnitude of DSE was significantly higher in interneurons compared with pyramidal cells, though developed with some latency

The Effects of COVID-19 on Counselor-in-Training Resilience: A Case Study

Contemporary literature in counseling suggests that resilience is a protective factor in preventing burnout among counselors and counselors-in-training. The strategies that counseling students have historically relied on to learn resilient habits have been disrupted by the COVID-19 pandemic, but the implications for students are still unknown. This qualitative case study examined the impact of the COVID-19 pandemic on 17 counselors-in-training, their adjustments through a resilience lens, and students’ perspectives on the response of their program in support of pandemic-related challenges. Findings of the current study pinpoint specific causes of counseling students’ psychological distress, as well as the social and academic ramifications. Findings also highlight coping strategies that may increase resilience among counselors-in-training. Implications and recommendations for counseling programs are included

FLEXIQinase, a mass spectrometry-based assay, to unveil multi-kinase mechanisms

We introduce a mass spectrometry-based method that provides residue-resolved quantitative information about protein phosphorylation. In this FLEXIQinase assay we combined our Full-Length Expressed Stable Isotope-labeled Protein for Quantification strategy (FLEXIQuant) with a traditional kinase assay to determine the mechanisms of multi-kinase substrate phosphorylation such as priming-dependent kinase activities. The assay monitors the decrease in signal intensity of the substrate peptides and the concomitant increase in the (n×80 Da)-shifted phosphorylated peptide. We analyzed the c-Jun N-terminal Kinase (JNK)-dependent glycogen synthase kinase 3β (GSK3β) activity on doublecortin (DCX) revealing mechanistic details about the role of phosphorylation cross-talk in GSK3β activity and permitting an advanced model for GSK3β-mediated signaling

Cellular and molecular characterization of multiplex autism in human induced pluripotent stem cell-derived neurons

Background: Autism spectrum disorder (ASD) is a neurodevelopmental disorder with pronounced heritability in the general population. This is largely attributable to the effects of polygenic susceptibility, with inherited liability exhibiting distinct sex differences in phenotypic expression. Attempts to model ASD in human cellular systems have principally involved rare de novo mutations associated with ASD phenocopies. However, by definition, these models are not representative of polygenic liability, which accounts for the vast share of population-attributable risk. Methods: Here, we performed what is, to our knowledge, the first attempt to model multiplex autism using patient-derived induced pluripotent stem cells (iPSCs) in a family manifesting incremental degrees of phenotypic expression of inherited liability (absent, intermediate, severe). The family members share an inherited variant of uncertain significance (VUS) in Results: cExN neurospheres from the two affected individuals were reduced in size, compared to those derived from unaffected related and unrelated individuals. This reduction was, at least in part, due to increased apoptosis of cells from affected individuals upon initiation of cExN neural induction. Likewise, cIN neural progenitor cells from affected individuals exhibited increased apoptosis, compared to both unaffected individuals. Transcriptomic analysis of both cExN and cIN neural progenitor cells revealed distinct molecular signatures associated with affectation, including the misregulation of suites of genes associated with neural development, neuronal function, and behavior, as well as altered expression of ASD risk-associated genes. Conclusions: We have provided evidence of morphological, physiological, and transcriptomic signatures of polygenic liability to ASD from an analysis of cellular models derived from a multiplex autism family. ASD is commonly inherited on the basis of additive genetic liability. Therefore, identifying convergent cellular and molecular phenotypes resulting from polygenic and monogenic susceptibility may provide a critical bridge for determining which of the disparate effects of rare highly deleterious mutations might also apply to common autistic syndromes

A Novel Hap1-Tsc1 interaction regulates neuronal mTORC1 signaling and morphogenesis in the brain

Tuberous sclerosis complex (TSC) is a leading genetic cause of autism. The TSC proteins Tsc1 and Tsc2 control the mTORC1 signaling pathway in diverse cells, but how the mTORC1 pathway is specifically regulated in neurons remains to be elucidated. Here, using an interaction proteomics approach in neural cells including neurons, we uncover the brain-enriched protein huntingtin-associated protein 1 (Hap1) as a novel functional partner of Tsc1. Knockdown of Hap1 promotes specification of supernumerary axons in primary hippocampal neurons and profoundly impairs the positioning of pyramidal neurons in the mouse hippocampus in vivo. The Hap1 knockdown-induced phenotypes in primary neurons and in vivo recapitulate the phenotypes induced by Tsc1 knockdown. We also find that Hap1 knockdown in hippocampal neurons induces the downregulation of Tsc1 and stimulates the activity of mTORC1, as reflected by phosphorylation of the ribosomal protein S6. Inhibition of mTORC1 activity suppresses the Hap1 knockdown-induced polarity phenotype in hippocampal neurons. Collectively, these findings define a novel link between Hap1 and Tsc1 that regulates neuronal mTORC1 signaling and neuronal morphogenesis, with implications for our understanding of developmental disorders of cognition

Cortico-cortical stimulation and robot-assisted therapy (CCS and RAT) for upper limb recovery after stroke: study protocol for a randomised controlled trial

Background: Since birth, during the exploration of the environment to interact with objects, we exploit both the motor and sensory components of the upper limb (UL). This ability to integrate sensory and motor information is often compromised following a stroke. However, to date, rehabilitation protocols are focused primarily on recovery of motor function through physical therapies. Therefore, we have planned a clinical trial to investigate the effect on functionality of UL after a sensorimotor transcranial stimulation (real vs sham) in add-on to robot-assisted therapy in the stroke population. Methods: A randomised double-blind controlled trial design involving 32 patients with a single chronic stroke (onset > 180 days) was planned. Each patient will undergo 15 consecutive sessions (5 days for 3 weeks) of paired associative stimulation (PAS) coupled with UL robot-assisted therapy. PAS stimulation will be administered using a bifocal transcranial magnetic stimulator (TMS) on the posterior-parietal cortex and the primary motor area (real or sham) of the lesioned hemisphere. Clinical, kinematics and neurophysiological changes will be evaluated at the end of protocol and at 1-month follow-up and compared with baseline. The Fugl-Meyer assessment scale will be the primary outcome. Secondly, kinematic variables will be recorded during the box-and-block test and reaching tasks using video analysis and inertial sensors. Single pulse TMS and electroencephalography will be used to investigate the changes in local cortical reactivity and in the interconnected areas. Discussion: The presented trial shall evaluate with a multimodal approach the effects of sensorimotor network stimulation applied before a robot-assisted therapy training on functional recovery of the upper extremity after stroke. The combination of neuromodulation and robot-assisted therapy can promote an increase of cortical plasticity of sensorimotor areas followed by a clinical benefit in the motor function of the upper limb. Trial registration: ClinicalTrials.gov NCT05478434. Registered on 28 Jul 2022

Regional Precuneus Cortical Hyperexcitability in Alzheimer's Disease Patients

Objective: Neuronal excitation/inhibition (E/I) imbalance is a potential cause of neuronal network malfunctioning in Alzheimer's disease (AD), contributing to cognitive dysfunction. Here, we used a novel approach combining transcranial magnetic stimulation (TMS) and electroencephalography (EEG) to probe cortical excitability in different brain areas known to be directly involved in AD pathology. Methods: We performed TMS-EEG recordings targeting the left dorsolateral prefrontal cortex (l-DLPFC), the left posterior parietal cortex (l-PPC), and the precuneus (PC) in a large sample of patients with mild-to-moderate AD (n = 65) that were compared with a group of age-matched healthy controls (n = 21). Results: We found that patients with AD are characterized by a regional cortical hyperexcitability in the PC and, to some extent, in the frontal lobe, as measured by TMS-evoked potentials. Notably, cortical excitability assessed over the l-PPC was comparable between the 2 groups. Furthermore, we found that the individual level of PC excitability was associated with the level of cognitive impairment, as measured with Mini-Mental State Examination, and with corticospinal fluid levels of Aβ42 . Interpretation: Our data provide novel evidence that precuneus cortical hyperexcitability is a key feature of synaptic dysfunction in patients with AD. The current results point to the combined approach of TMS and EEG as a novel promising technique to measure hyperexcitability in patients with AD. This index could represent a useful biomarker to stage disease severity and evaluate response to novel therapies. ANN NEUROL 2022

Selective targeting of activating and inhibitory Smads by distinct WWP2 ubiquitin ligase isoforms differentially modulates TGFβ signalling and EMT

Ubiquitin-dependent mechanisms have emerged as essential regulatory elements controlling cellular levels of Smads and TGFß-dependent biological outputs such as epithelial–mesenchymal transition (EMT). In this study, we identify a HECT E3 ubiquitin ligase known as WWP2 (Full-length WWP2-FL), together with two WWP2 isoforms (N-terminal, WWP2-N; C-terminal WWP2-C), as novel Smad-binding partners. We show that WWP2-FL interacts exclusively with Smad2, Smad3 and Smad7 in the TGFß pathway. Interestingly, the WWP2-N isoform interacts with Smad2 and Smad3, whereas WWP2-C interacts only with Smad7. In addition, WWP2-FL and WWP2-C have a preference for Smad7 based on protein turnover and ubiquitination studies. Unexpectedly, we also find that WWP2-N, which lacks the HECT ubiquitin ligase domain, can also interact with WWP2-FL in a TGFß-regulated manner and activate endogenous WWP2 ubiquitin ligase activity causing degradation of unstimulated Smad2 and Smad3. Consistent with our protein interaction data, overexpression and knockdown approaches reveal that WWP2 isoforms differentially modulate TGFß-dependent transcription and EMT. Finally, we show that selective disruption of WWP2 interactions with inhibitory Smad7 can stabilise Smad7 protein levels and prevent TGFß-induced EMT. Collectively, our data suggest that WWP2-N can stimulate WWP2-FL leading to increased activity against unstimulated Smad2 and Smad3, and that Smad7 is a preferred substrate for WWP2-FL and WWP2-C following prolonged TGFß stimulation. Significantly, this is the first report of an interdependent biological role for distinct HECT E3 ubiquitin ligase isoforms, and highlights an entirely novel regulatory paradigm that selectively limits the level of inhibitory and activating Smads