Sorghum is an important food and feed crop in the dry lowland areas of Ethiopia. Farmers grow both early-sown long-duration landraces and late-sown short-duration improved varieties. Because timing and intensity of drought stress can vary in space and time, an understanding of major traits (G), environments (E), management (M), and their interactions (G×E×M) is needed to optimize grain and forage yield given the limited available resources. Crop simulation modeling can provide insights into these complex G×E×M interactions and be used to identify possible avenues for adaptation to prevalent drought patterns in Ethiopia. In a previous study predictive phenology models were developed for a range of Ethiopian germplasm. In this study, the aims were to (1) further parameterize and validate the APSIM-sorghum model for crop growth and yield of Ethiopian germplasm, and (2) quantify by simulation the productivity-risk trade-offs associated with early vs late sowing strategies in the dry lowlands of Ethiopia. Field experiments involving Ethiopian germplasm with contrasting phenology and height were conducted under well-watered (Melkassa) and water-limited (Miesso) conditions and crop development, growth and yield measured. Soil characterization and weather records at the experimental sites, combined with model parameterization, enabled testing of the APSIM-sorghum model, which showed good correspondence between simulated and observed data. The simulated productivity for the Ethiopian dry lowlands environments showed trade-offs between biomass and grain yield for early and late sowing strategies. The late sowing strategy tended to produce less biomass except in poor seasons, whereas it tended to produce greater grain yield except in very good seasons. This study exemplified the systems approach to identifying traits and management options needed to quantify the production-risk trade-offs associated with crop adaptation in the Ethiopian dry lowlands and further exemplifies the general robustness of the sorghum model in APSIM for this task.

Genetic variation in the transcription factor 4 ( TCF4) gene is associated with risk for a variety of developmental and psychiatric conditions, which includes a syndromic form of ASD called Pitt Hopkins Syndrome (PTHS). TCF4 encodes an activity-dependent transcription factor that is highly expressed during cortical development and in animal models is shown to regulate various aspects of neuronal development and function. However, our understanding of how disease-causing mutations in TCF4 confer pathophysiology in a human context is lacking. Here we show that cortical neurons derived from patients with TCF4 mutations have deficits in spontaneous synaptic transmission, network excitability and homeostatic plasticity. Transcriptomic analysis indicates these phenotypes result from altered expression of genes involved in presynaptic neurotransmission and identifies the presynaptic binding protein, RIMBP2 as the most differentially expressed gene in PTHS neurons. Remarkably, TCF4-dependent deficits in spontaneous synaptic transmission and network excitability were rescued by increasing RIMBP2 expression in presynaptic neurons. Together, these results identify TCF4 as a critical transcriptional regulator of human synaptic development and plasticity and specifically identifies dysregulation of presynaptic function as an early pathophysiology in PTHS.

Social touch, an important aspect of social interaction and communication, is essential to kinship across animal species. How animals experience and respond to social touch has not been thoroughly investigated, in part due to the lack of appropriate assays. Previous studies that examined social touch in freely moving rodents lacked the necessary temporal and spatial control over individual touch interactions. We designed a novel head-fixed assay for social touch in mice, in which the experimenter has complete control to elicit highly stereotyped bouts of social touch between two animals. The user determines the number, duration, context, and type of social touch interactions, while monitoring with high frame rate cameras an array of complex behavioral responses. We focused on social touch to the face because of their high translational relevance to humans. We validated this assay in two different models of autism spectrum disorder (ASD), the Fmr1 knockout model of Fragile X Syndrome and maternal immune activation mice. We observed increased avoidance, hyperarousal, and more aversive facial expressions to social touch, but not to object touch, in both ASD models compared to controls. Because this new social touch assay for head-fixed mice can be used to record neural activity during repeated bouts of social touch it should be of interest to neuroscientists interested in uncovering the underlying circuits.

δ-catenin is expressed in excitatory synapses and functions as an anchor for the glutamatergic AMPA receptor (AMPAR) GluA2 subunit in the postsynaptic density. The glycine 34 to serine (G34S) mutation in the δ-catenin gene is found in autism spectrum disorder (ASD) patients and induces loss of δ-catenin functions at excitatory synapses, which is presumed to underlie ASD pathogenesis in humans. However, how the G34S mutation causes loss of δ-catenin functions to induce ASD remains unclear. Here, using neuroblastoma cells, we discover that the G34S mutation generates an additional phosphorylation site for glycogen synthase kinase 3β (GSK3β). This promotes δ-catenin degradation and causes the reduction of δ-catenin levels, which likely contributes to the loss of δ-catenin functions. Synaptic δ-catenin and GluA2 levels in the cortex are significantly decreased in mice harboring the δ-catenin G34S mutation. The G34S mutation increases glutamatergic activity in cortical excitatory neurons while it is decreased in inhibitory interneurons, indicating changes in cellular excitation and inhibition. δ-catenin G34S mutant mice also exhibit social dysfunction, a common feature of ASD. Most importantly, inhibition of GSK3β activity reverses the G34S-induced loss of δ-catenin function effects in cells and mice. Finally, using δ-catenin knockout mice, we confirm that δ-catenin is required for GSK3β inhibition-induced restoration of normal social behaviors in δ-catenin G34S mutant animals. Taken together, we reveal that the loss of δ-catenin functions arising from the ASD-associated G34S mutation induces social dysfunction via alterations in glutamatergic activity and that GSK3β inhibition can reverse δ-catenin G34S-induced synaptic and behavioral deficits.

Social anxiety disorder (SAD) and autism spectrum disorder (ASD) are highly overlapping in symptoms and have a high rate of comorbidity, posing challenges in diagnosis and intervention for both disorders. Both disorders are linked to abnormal attention to the eyes, yet how they interactively modulate the attentional process to the eyes remains unclear.

Emotion dysregulation is common among individuals with autism spectrum disorder (ASD). This study examined the relationship between emotion dysregulation and resting heart rate variability (HRV), a marker of the autonomic nervous system, in ASD adolescents. Resting HRV data were collected from ASD (n = 23) and typically developing (TD) adolescents (n = 32) via short-term electrocardiogram. Parents/caregivers reported participants' level of emotion dysregulation with the Emotion Dysregulation Inventory (EDI). Controlling for the effects of age and gender, regression analyses revealed moderating effects of group, suggesting that lower resting HRV was more strongly associated with greater emotion dysregulation in ASD than TD adolescents. The results support the view that disruptions in autonomic functioning may contribute to emotion dysregulation in ASD.

Autism spectrum disorder (ASD) is a heterogeneous group of early-onset neurodevelopmental disorders known to be highly heritable with a complex genetic architecture. Abnormal brain developmental trajectories that impact synaptic functioning, excitation-inhibition balance and brain connectivity are now understood to play a central role in ASD. Ongoing efforts to identify the genetic underpinnings still prove challenging, in part due to phenotypic and genetic heterogeneity.This review focuses on parent-of-origin effects (POEs), where the phenotypic effect of an allele depends on its parental origin. POEs include genomic imprinting, transgenerational effects, mitochondrial DNA, sex chromosomes and mutational transmission bias. The motivation for investigating these mechanisms in ASD has been driven by their known impacts on early brain development and brain functioning, in particular for the most well-documented POE, genomic imprinting. Moreover, imprinting is implicated in syndromes such as Angelman and Prader-Willi, which frequently share comorbid symptoms with ASD. In addition to other regions in the genome, this comprehensive review highlights the 15q11-q13 and 7q chromosomal regions as well as the mitochondrial DNA as harbouring the majority of currently identified POEs in ASD.

The growing prevalence of neurological disorders, e.g., Autism Spectrum Disorder (ASD), demands robust computer-aided diagnosis (CAD) due to the diverse symptoms which require early intervention, particularly in young children. The absence of a benchmark neuroimaging diagnostics paves the way to study transitions in the brain's anatomical structure and neurological patterns associated with ASD. The existing CADs take advantage of the large-scale baseline dataset from the Autism Brain Imaging Data Exchange (ABIDE) repository to improve diagnostic performance, but the involvement of multisite data also amplifies the variabilities and heterogeneities that hinder satisfactory results. To resolve this problem, we propose a Deep Multimodal Neuroimaging Framework (DeepMNF) that employs Functional Magnetic Resonance Imaging (fMRI) and Structural Magnetic Resonance Imaging (sMRI) to integrate cross-modality spatiotemporal information by exploiting 2-dimensional time-series data along with 3-dimensional images. The purpose is to fuse complementary information that increases group differences and homogeneities. To the best of our knowledge, our DeepMNF achieves superior validation performance than the best reported result on the ABIDE-1 repository involving datasets from all available screening sites. In this work, we also demonstrate the performance of the studied modalities in a single model as well as their possible combinations to develop the multimodal framework.

Neuronal migration and morphogenesis are fundamental processes for cortical development. Their defects may cause abnormities in neural circuit formation and even neuropsychiatric disorders. Many proteins, especially layer-specific transcription factors and adhesion molecules, have been reported to regulate the processes. However, the involvement of non-coding RNAs in cortical development has not been extensively studied. Here, we identified microRNA-218 (miR-218) as a layer V-specific microRNA in mouse brains. Expression of miR-218 was elevated in patients with autism spectrum disorder (ASD) and schizophrenia. We found in this study that miR-218 overexpression in developing mouse cortex led to severe defects in radial migration, morphogenesis, and spatial distribution of the cortical neurons. Moreover, we identified Satb2, an upper-layer marker, as a molecular target repressed by miR-218. These results suggest an underlying mechanism of miR-218 involvement in neuropsychiatric disorders, and the interactions of layer-specific non-coding RNAs and proteins in regulating cortical development.

The labial gland is a major exocrine gland in the thoracic cavity of ants, which is connected to the mouth area and opens at the base of the labium. The labial gland in the various castes and males of Camponotus japonicus were examined using dissection, light microscopy, scanning and transmission electron microscopy. Our findings reveal clear caste differences in the appearance of the labial gland, and suggest a relationship between gland structure and its behavioral role in queens, males and workers: queens possess the largest reservoir sac; males have the smallest; workers have abundant secretion droplets in the gland cells of the tubules; epithelial thickness of gland cells varies considerably between workers and reproductive ants. The apical cell region has a high density of microvilli and polymorphic mitochondria, whereas the central cell region is rich in rough endoplasmic reticulum (RER) which means its main secretions are proteinaceous compounds. We believe that the labial gland has a different function in the castes of C. japonicus: the gland of workers and queens may be used to feed the larvae; workers participate in trophallaxis in the nest, while the males are not involved in these activities. Calculations of the relative size of the labial gland for each caste and males indicated that minor workers have the relative highest developed labial gland, supporting a role in trophallaxis. In addition, we found a phenomenon of enlarged labial gland in minor workers, which accounted for almost 22%, but the reason for this is unknown.

Miniaturization is one of the important trends in the evolution of terrestrial arthropods. In order to study adaptations to microscopic sizes, the anatomy of the smallest insects was previously studied, but not the anatomy of the smallest mites. Some of the smallest mites are Eriophyidae. In this study we describe for the first time the anatomy of the mite Achaetocoptes quercifolii, which is about 115 μm long. For this purpose, we used light, scanning, and transmission electron microscopy and performed 3D reconstructions. The anatomy of A. quercifolii is compared with the anatomy of larger representatives of Eriophyoidea. Despite the small size of the studied species, there is no considerable simplification of its anatomy compared to larger four-legged mites. A. quercifolii has a number of miniaturization effects similar to those found in microinsects: a strong increase in the relative volume of the reproductive system, an increase in the relative volume of the brain, reduction in the number and size of cells of the nervous system. As in some larger four-legged mites, A. quercifolii undergoes midgut lysis at the stage of egg production. On the other hand, in A. quercifolii a greater number of opisthosomal muscles are preserved than in larger gall-forming four-legged mites.

The Bittacidae are unique in holometabolous insects in that their larvae bear a dorsal ocellus on the frons. The fine structure of the dorsal ocellus, however, has not been investigated to date. Here, the ultrastructure of the larval dorsal ocellus was studied in the hangingfly Bittacus planus Cheng, 1949 using light, scanning, and transmission electron microscopy. The dorsal ocellus of the larvae comprises a cornea, corneagenous cells, and retinula cells. The cornea is a laminated structure. A layer of corneagenous cells is located below the cornea. Numerous retinula cells are arranged tightly beneath the corneagenous cells. The retinula cells modify their adjacent membranes into numerous linear microvilli, which form an analogue of the rhabdom among adjacent retinula cells. The results show that the dorsal ocellus of larval Bittacidae is a highly vestigial organ and appears to be degenerating during the postembryonic development. The presence of the vestigial dorsal ocellus is likely to represent an ancestral plesiomorphy of holometabolous insects, providing new evidence for exploring the evolutionary origin of holometabolous larvae.

Preterm birth has been linked with increased incidence of autism spectrum disorder (ASD). Despite the remarkable difference in the clinical backgrounds between ASD children born preterm and term, cross-sectional studies have found no striking difference in their autistic traits. To highlight autistic traits related with preterm birth, children born very preterm (prospective birth cohort, n = 50) and term (case cohort, n = 16), who were diagnosed as "Autism" by the Autism Diagnostic Observation Schedule (ADOS), 2nd edition, were compared using the calibrated severity scores of ADOS-2 and T-scores of the Social Responsiveness Scale, 2nd edition. No significant difference was found in the calibrated severity scores between ASD children born preterm and term. There was a trend that T-scores were smaller for the preterm cohort, which did not reach a statistical significance. Even when detailed cross-sectional information was obtained using ADOS-2, no difference in autistic traits was observed between children born very preterm and term. Our findings were consistent with a previous study, which assessed the entire prospective cohort of children born very preterm and found no difference in original ADOS scores. Further studies are warranted to delineate how preterm birth affects the autistic traits and their parental perception in a large prospective cohort.

It is now recognised that autism spectrum disorder (ASD) and personality disorders (PDs) have a variety of factors in common. However, the exact nature of the relationship between ASD and the PDs remains unclear. The overlapping symptom profiles of ASD and PDs can lead to diagnostic uncertainty - features of ASD and PD can be misattributed and easily lead to misdiagnosis of ASD patients. Since differentiating between ASD and PD is such a complex task, it has been argued that there is a need for additional understanding and markers for facilitating diagnostic procedures. There is an urgent need to explore, first, how clinicians make diagnostic decisions and, second, how to effectively deal with the challenges and difficulties they face when making decisions. Also, where there are clear overlaps, how do clinicians choose how to attribute labels in order to understand the person.

Background: Atypical eating behaviors and feeding issues are common in children with autism spectrum disorder (ASD). Aim: This study aims to evaluate the nutritional status and eating behavior of the ASD and typically developing groups. Methods: A case-control study was conducted from January to April 2019 in Nghe An, Vietnam. A total of 93 children in each group participated in the study with their main caregivers. We applied the Children's Eating Behavior Inventory (CEBI) to evaluate the eating behaviors of children. Results: Overweight and obesity in ASD children accounted for 41.9%. The CEBI score and %CEBI of the ASD group was higher than that of the control group (104.0 ± 14.2 and 91.3 ± 8.3; 24.1 ± 21.4 and 5.0 ± 11.8, respectively). Most of the adverse mealtime behaviors of ASD children focused on excessive duration (52.7%), distraction (40.9%), and food refusal (39.8%). In total 88.2% of caregivers had to comfort their ASD children at every meal, followed by threatening, scolding, or punishing children if they refused to eat (57.0%). Conclusion: Being overweight/obese and having eating behavior difficulties were prevalent among ASD children in Vietnam. Safer alternatives, such as lifestyle measures and seeking help from a nutritional therapist, can help ASD children reduce weight and modify their erroneous feeding habits.

Compound eyes are the prominent visual organs of insects and can provide valuable information for the reconstruction of insect phylogeny. Although the largest butterfly family (Nymphalidae) has been well defined, the infrafamilial phylogenetic relationships remain controversial hitherto. In the present study the ultrastructure of the compound eyes of three nymphalids Neptis beroe, Childrena zenobia, and Palaeonympha opalina was investigated using light and transmission electron microscopy in an attempt to seek potentially important phylogenetic characters. The compound eyes of the nymphalids share a tracheal system in a "1-4-8" branching pattern. The eight tracheal subbranches exhibit distinct distribution patterns along the basal retinula cell as follows: the tracheal subbranches of Palaeonympha opaline are close to the rhabdom in the distance from the distalmost part of the basal retinula cell to the rhabdom end, while those of N. beroe and C. zenobia are on the periphery of the retinula along almost the whole basal retinula cell and become close to the rhabdom just at the proximal end of the basal retinula cell. The tracheal structure of the three nymphalids is discussed for their potential phylogenetic implications.

Autism spectrum disorder (ASD) is one common psychiatric illness that manifests in neurological and developmental disorders, which can last throughout a person's life and cause challenges in social interaction, communication, and behavior. Since the standard ASD diagnosis is highly based on the symptoms of the disease, it is difficult to make an early diagnosis to take the best cure opportunity. Compared to the standard methods, functional brain network (FBN) could reveal the statistical dependence among neural architectures in brains and provide potential biomarkers for the early neuro-disease diagnosis and treatment of some neurological disorders. However, there are few FBN estimation methods that take into account the noise during the data acquiring process, resulting in poor quality of FBN and thus poor diagnosis results. To address such issues, we provide a brand-new approach for estimating FBNs under a noise modeling framework. In particular, we introduce a noise term to model the representation errors and impose a regularizer to incorporate noise prior into FBNs estimation. More importantly, the proposed method can be formulated as conducting traditional FBN estimation based on transformed fMRI data, which means the traditional methods can be elegantly modified to support noise modeling. That is, we provide a plug-and-play noise module capable of being embedded into different methods and adjusted according to different noise priors. In the end, we conduct abundant experiments to identify ASD from normal controls (NCs) based on the constructed FBNs to illustrate the effectiveness and flexibility of the proposed method. Consequently, we achieved up to 13.04% classification accuracy improvement compared with the baseline methods.

The number of children diagnosed with autism spectrum disorders (ASD) worldwide has increased rapidly in the past decade and China is no exception. Yet the identity development of Chinese parents of children with ASD is little understood. This study employed an ethics of care perspective to explore the identity of parents of children with ASD as shaped in their social-cultural context in mainland China.

The GRIN2B-related neurodevelopmental disorder is a rare disease caused by mutations in the GRIN2B gene, which encodes the GluN2B subunit of NMDA receptors. Most individuals with GRIN2B-related neurodevelopmental disorder present with intellectual disability and developmental delay. Motor impairments, autism spectrum disorder, and epilepsy are also common. A large number of pathogenic de novo mutations have been identified in GRIN2B. However, it is not yet known how these variants lead to the clinical symptoms of the disease. Recent research has begun to address this issue. Here, we describe key experimental approaches that have been used to better understand the pathophysiology of this disease. We discuss the impact of several distinct pathogenic GRIN2B variants on NMDA receptor properties. We then critically review pivotal studies examining the synaptic and neurodevelopmental phenotypes observed when disease-associated GluN2B variants are expressed in neurons. These data provide compelling evidence that various GluN2B mutants interfere with neuronal differentiation, dendrite morphogenesis, synaptogenesis, and synaptic plasticity. Finally, we identify important open questions and considerations for future studies aimed at understanding this complex disease. Together, the existing data provide insight into the pathophysiological mechanisms that underlie GRIN2B-related neurodevelopmental disorder and emphasize the importance of comparing the effects of individual, disease-associated variants. Understanding the molecular, cellular and circuit phenotypes produced by a wide range of GRIN2B variants should lead to the identification of core neurodevelopmental phenotypes that characterize the disease and lead to its symptoms. This information could help guide the development and application of effective therapeutic strategies for treating individuals with GRIN2B-related neurodevelopmental disorder.