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The role of selective new generation bioisecticides, beside their effectiveness against key pests, relies on their safety to beneficial arthropods. Spinetoram, a semi-synthetic analogue of the microbial-derived bioinsecticide spinosad is registered worldwide for application in numerous crops, but assessment of its ecotoxicological risk to beneficial arthropods has scarcely been documented. Moreover, this is the first report on toxic effects of spinetoram on a pest, the greenhouse whitefly Trialeurodes vaporariorum Westwood (Hemiptera: Aleyrodidae), and/or its successful biocontrol agent, the parasitoid Encarsia formosa Gahan (Hymenoptera: Aphelinidae). Under laboratory conditions, we assessed the acute toxicity of spinetoram insecticide (25% a.i.) to adults, nymphs and eggs of the greenhouse whitefly, as well as to parasitoid adults and pupae. In all concentration-response bioassays, the spinetoram insecticide was applied to tobacco leaves settled onto 1% agar layer in ventilated Petri dishes using a Potter spray tower. The parameters of spinetoram acute toxicity to adults of both the pest and the parasitoid were evaluated in residual contact bioassays, while whitefly eggs and nymphs, and parasitoid pupae were topically treated with a series of spinetoram concentrations, covering a range of 10-90% mortality. Lethal spinetoram effects on the parasitoid E. formosa were assessed through selectivity ratio (SR) estimations, showing the ratios beetween median lethal concentrations (LC50s) estimated for the parasitoid, and LC50s estimated for the pest. The following LC50 values were obtained: 4.593, 15.027 and 11.73 mg A.I./l for whitefly adults, nymphs and eggs, respectively, and 0.686 and 1.715 mg A.I./l for parasitoid adults and pupae, respectively. The calculated SR estimations were below 1, indicating that spinetoram insecticide is non-selective to both tested stages of the parasitoid E. formosa. A more detailed understanding of spinetoram impact on E. formosa in whitefly integrated management requires further evaluation of sublethal effects and greenhouse trials, with an emphasis on population-level responses.

Background: Although the pupal parasitoid Trichopria drosophilae is used in conservative and augmentative biocontrol of Drosophila suzukii infestations, current pest management strategies mostly rely on multiple insecticide applications. In this context, the aim of the study was to investigate the baseline toxicity of nine insecticides on D. suzukii larvae and their multiple sublethal effects (LC10) on immature stages of the pest feeding on contaminated diet and T. drosophilae developing within the intoxicated host. Results: Chlorpyriphos and azadirachtin showed the lowest and the highest LC10, the values of which were 9.78 × 1013 and 1.46 × 103 times lower than their recommended label field rate, respectively. Among tested insecticides, imidacloprid, malathion and dimethoate were the only treatments that did not affect the juvenile development time of D. suzukii, while spinosad and the organophosphates chlorpyriphos and dimethoate did not influence fly pupal size. No sublethal effects were recorded on T. drosophilae degree of infestation (DI) and juvenile development time. On the contrary, cyazypyr and dimethoate negatively affected the success of parasitism (SP) and the number of progeny of the pupal parasitoid, in association with malathion for the first parameter and spinosad for the fertility. Compared to the untreated control, more female progeny emerged following azadirachtin exposure, while dimethoate caused the opposite effect. Imidacloprid, lambda‐cyhalothrin and spinetoram decreased hind tibia length of emerged parasitoids. Conclusion: This study provides new insights on the (eco)toxicological profile of nine insecticides and new information needed to support the deployment of T. drosophilae in the field within the sustainable management techniques against D. suzukii. © 2023 The Authors. Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry. [ABSTRACT FROM AUTHOR]

Our visual system extracts the emotional meaning of human facial expressions rapidly and automatically. Novel paradigms using fast periodic stimulations have provided insights into the electrophysiological processes underlying emotional content extraction: the regular occurrence of specific identities and/or emotional expressions alone can drive diagnostic brain responses. Consistent with a processing advantage for social cues of threat, we expected angry facial expressions to drive larger responses than neutral expressions. In a series of four EEG experiments, we studied the potential boundary conditions of such an effect: (i) we piloted emotional cue extraction using 9 facial identities and a fast presentation rate of 15 Hz (N = 16); (ii) we reduced the facial identities from 9 to 2, to assess whether (low or high) variability across emotional expressions would modulate brain responses (N = 16); (iii) we slowed the presentation rate from 15 Hz to 6 Hz (N = 31), the optimal presentation rate for facial feature extraction; (iv) we tested whether passive viewing instead of a concurrent task at fixation would play a role (N = 30). We consistently observed neural responses reflecting the rate of regularly presented emotional expressions (5 Hz and 2 Hz at presentation rates of 15 Hz and 6 Hz, respectively). Intriguingly, neutral expressions consistently produced stronger responses than angry expressions, contrary to the predicted processing advantage for threat-related stimuli. Our findings highlight the influence of physical differences across facial identities and emotional expressions. [ABSTRACT FROM AUTHOR]

Highlights: [•] Steady-state evoked potentials (SSEPs) indexed concurrent visuo-tactile processing. [•] Inter-modal selective attention influenced SSEP amplitude and phase. [•] Patterns of SSEP modulation differed between vision and touch. [Copyright &y& Elsevier]

Late-stage neuropathological hallmarks of Alzheimer's disease (AD) are b-amyloid (bA) and hyperphosphorylated tau peptides, aggregated into plaques and tangles, respectively. Corresponding phenotypes have been mimicked in existing transgenic mice, however, the translational value of aggressive over-expression has recently been questioned. As controlled gene expression may offer animal models with better predictive validity, we set out to design a transgenic mouse model that circumvents complications arising from pronuclear injection and massive over-expression, by targeted insertion of human mutated amyloid and tau transgenes, under the forebrain- and neurone-specific CaMKIIa promoter, termed PLB1Double. Crossing with an existing presenilin 1 line resulted in PLB1Triple mice. PLB1Triple mice presented with stable gene expression and age-related pathology of intra-neuronal amyloid and hyperphosphorylated tau in hippocampus and cortex from 6 months onwards. At this early stage, pre-clinical 18FDG PET/CT imaging revealed cortical hypometabolism with increased metabolic activity in basal forebrain and ventral midbrain. Quantitative EEG analyses yielded heightened delta power during wakefulness and REM sleep, and time in wakefulness was already reliably enhanced at 6 months of age. These anomalies were paralleled by impairments in long-term and short-term hippocampal plasticity and preceded cognitive deficits in recognition memory, spatial learning, and sleep fragmentation all emerging at ,12 months. These data suggest that prodromal AD phenotypes can be successfully modelled in transgenic mice devoid of fibrillary plaque or tangle development. PLB1Triple mice progress from a mild (MCI-like) state to a more comprehensive AD-relevant phenotype, which are accessible using translational tools such as wireless EEG and microPET/CT. [ABSTRACT FROM AUTHOR]

TGF-β-receptor 2 (TGFBR2) gene defects have been recently associated with Marfan syndrome (MFS) with prominent cardio-skeletal phenotype in patients with negative fibrillin-1 (FBN1) gene screening. Four mutations have been identified to date in five unrelated families. We screened TGFBR2 gene by direct automated sequencing in two adult patients diagnosed with MFS according to Ghent criteria, and in one girl clinically suspected as affected on the basis of a major cardiovascular criterion and skeletal involvement, all proven not to carry mutations in the exon–intron boundaries of FBN1 gene. We identified two novel and one known TGFBR2 gene mutations in the three unrelated probands. The D446N was identified in a 4-year-old girl with de novo disease characterized by severe cardiovascular disease and skeletal involvement. The M425V and R460H mutations were identified in two familial, autosomal dominant MFSs, both characterized by major cardio-skeletal signs and absence of major ocular signs. The mutation R460H has been recently reported in a family with thoracic aortic aneurysms and dissection. The three mutations are absent in 192 controls and affect evolutionarily conserved residues of the serine/threonine kinase domain (exon 5). Our data support the recently reported association between TGFBR2 gene and MFS without major ocular signs (MFS2). The number of genotyped cases however is too low to confirm that major ocular signs are characteristically absent in MFS2. Accordingly, all patients proven or suspected to be affected by MFS with negative FBN1 gene screening could benefit from rapid investigation of the TGFBR2 gene.European Journal of Human Genetics (2006) 14, 34–38. doi:10.1038/sj.ejhg.5201502; published online 12 October 2005 [ABSTRACT FROM AUTHOR]

Naturalistic learning scenarios are characterized by infrequent experience of external feedback to guide behavior. Higher-order learning mechanisms like second-order conditioning (SOC) may allow stimuli that were never experienced together with reinforcement to acquire motivational value. Despite its explanatory potential for real-world learning, surprisingly little is known about the neural mechanism underlying such associative transfer of value in SOC. Here, we used multivariate cross-session, cross-modality searchlight classification on functional magnetic resonance imaging data obtained from humans during SOC. We show that visual first-order conditioned stimuli (CS) reinstate cortical patterns representing previously paired gustatory outcomes in the lateral orbitofrontal cortex (OFC). During SOC, this OFC region showed increased functional covariation with amygdala, where neural pattern similarity between second-order CS and outcomes increased from early to late stages of SOC. Our data suggest a mechanism by which motivational value is conferred to stimuli that were never paired with reinforcement., (© The Author(s) 2021. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)