Weberdissing3733

Autism spectrum disorder (ASD) is more prevalent in males than in females, but the neurobiological mechanisms that give rise to this sex-bias are poorly understood. The female protective hypothesis suggests that the manifestation of ASD in females requires higher cumulative genetic and environmental risk relative to males. Here, we test this hypothesis by assessing the additive impact of several ASD-associated OXTR variants on reward network resting-state functional connectivity in males and females with and without ASD, and explore how genotype, sex, and diagnosis relate to heterogeneity in neuroendophenotypes. Females with ASD who carried a greater number of ASD-associated risk alleles in the OXTR gene showed greater functional connectivity between the nucleus accumbens (NAcc; hub of the reward network) and subcortical brain areas important for motor learning. Relative to males with ASD, females with ASD and higher OXTR risk-allele-dosage showed increased connectivity between the NAcc, subcortical regions, and prefrontal brain areas involved in mentalizing. This increased connectivity between NAcc and prefrontal cortex mirrored the relationship between genetic risk and brain connectivity observed in neurotypical males showing that, under increased OXTR genetic risk load, females with ASD and neurotypical males displayed increased connectivity between reward-related brain regions and prefrontal cortex. These results indicate that females with ASD differentially modulate the effects of increased genetic risk on brain connectivity relative to males with ASD, providing new insights into the neurobiological mechanisms through which the female protective effect may manifest.Pseudogenes have long been considered as nonfunctional genomic sequences. Recent studies have shown that they can potentially regulate the expression of protein-coding genes and are dysregulated in diseases including cancer. However, the potential roles of pseudogenes in ovarian cancer have not been well studied. Here we characterized the pseudogene expression profile in HGSOC (high-grade serous ovarian carcinoma) by microarray. We identified 577 dysregulated pseudogenes and most of them were up-regulated (538 of 577). HMGA1P6 (High mobility group AT-hook 1 pseudogene 6) was one of the overexpressed pseudogenes and its expression was inversely correlated with patient survival. Mechanistically, HMGA1P6 promoted ovarian cancer cell malignancy by acting as a ceRNA (competitive endogenous RNA) that led to enhanced HMGA1 and HMGA2 expression. Importantly, HMGA1P6 was transcriptionally activated by oncogene MYC in ovarian cancer. Our findings reveal that MYC may contribute to oncogenesis through transcriptional regulation of pseudogene HMGA1P6 in ovarian cancer.The presence of both inversion (P) and time-reversal (T) symmetries in solids leads to a double degeneracy of the electronic bands (Kramers degeneracy). By lifting the degeneracy, spin textures manifest themselves in momentum space, as in topological insulators or in strong Rashba materials. The existence of spin textures with Kramers degeneracy, however, is difficult to observe directly. Here, we use quantum interference measurements to provide evidence for the existence of hidden entanglement between spin and momentum in the antiperovskite-type Dirac material Sr3SnO. We find robust weak antilocalization (WAL) independent of the position of EF. The observed WAL is fitted using a single interference channel at low doping, which implies that the different Dirac valleys are mixed by disorder. Notably, this mixing does not suppress WAL, suggesting contrasting interference physics compared to graphene. We identify scattering among axially spin-momentum locked states as a key process that leads to a spin-orbital entanglement.One key aspect of domain-general thought is the ability to integrate information across different cognitive domains. Here, we tested whether kea (Nestor notabilis) can use relative quantities when predicting sampling outcomes, and then integrate both physical information about the presence of a barrier, and social information about the biased sampling of an experimenter, into their predictions. Our results show that kea exhibit three signatures of statistical inference, and therefore can integrate knowledge across different cognitive domains to flexibly adjust their predictions of sampling events. This result provides evidence that true statistical inference is found outside of the great apes, and that aspects of domain-general thinking can convergently evolve in brains with a highly different structure from primates. This has important implications not only for our understanding of how intelligence evolves, but also for research focused on how to create artificial domain-general thought processes.Social learning is often proposed as an important driver of the evolution of human cooperation. In this view, cooperation in other species might be restricted because it mostly relies on individually learned or innate behaviours. Here, we show that juvenile cleaner fish (Labroides dimidiatus) can learn socially about cheating consequences in an experimental paradigm that mimics cleaners' cooperative interactions with client fish. Juvenile cleaners that had observed adults interacting with model clients learned to (1) behave more cooperatively after observing clients fleeing in response to cheating; (2) prefer clients that were tolerant to cheating; but (3) did not copy adults' arbitrary feeding preferences. These results confirm that social learning can play an active role in the development of cooperative strategies in a non-human animal. They further show that negative responses to cheating can potentially shape the reputation of cheated individuals, influencing cooperation dynamics in interaction networks.Genome-wide association study (GWAS) has determined the metabotropic glutamate receptor 7 (GRM7) gene as potential locus for schizophrenia risk variants; However, the relationship between the GRM7 variants and the risk of schizophrenia is still uncertain, and there are significant individual variations in response to the antipsychotic drugs. In order to identify susceptible gene and drug-response-related markers, 2413 subjects in our research were chosen for determining drug-response-related markers in schizophrenia. MitoSOXRed The rs1516569 variant (OR = 0.95, P  less then  3.47 × 10-4) was a significant risk factor, and a single-nucleotide polymorphism of GRM7 gene- rs9883258 (OR = 0.84, P = 2.18 × 10-3) has been determined as potential biomarkers for therapeutic responses of seven commonly used antipsychotic drugs (aripiprazole, haloperidol, olanzapine, perphenazine, quetiapine, risperidone and ziprasidone) in Chinese Han population; Significant associations with treatment response for several single-nucleotide polymorphisms in every antipsychotic drugs, such as rs779746 (OR = 1.