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The Fermi bubbles are two giant bubbles in gamma-rays lying above and below the Galactic Center (GC). Despite numerous studies on the bubbles, their origin and emission mechanism remain elusive. Here we use a suite of hydrodynamic simulations to study the scenario where the cosmic rays (CRs) in the bubbles are mainly accelerated at the forward shocks driven by a pair of opposing jets from Sgr A*. We find that an active galactic nucleus (AGN) jet event that happened 5–6 Myr ago can naturally reproduce the bilobular morphology of the bubbles, and the postshock gas temperature in the bubbles is heated to ∼0.4 keV, consistent with recent X-ray observations. The forward shocks compress the hot halo gas, and at low latitudes, the compressed gas shows an X-shaped structure, naturally explaining the biconical X-ray structure in the ROSAT 1.5 keV map in both morphology and X-ray surface brightness. CR acceleration is most efficient in the head regions of the bubbles during the first 2 Myr. The opposing jets release a total energy of ∼1055 erg with an Eddington ratio of ∼10−3, which falls well in the range of the hot accretion flow mode for black holes. Our simulations further show that the forward shocks driven by spherical winds at the GC typically produce bubbles with much wider bases than observed and could not reproduce the biconical X-ray structure at low latitudes. This suggests that starburst or AGN winds are unlikely the origin of the bubbles in the shock scenario.

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Motor control and learning impairments are common complications in individuals with autism spectrum disorder (ASD). Abnormal cerebellar development during critical phases may disrupt these motor functions and lead to autistic motor dysfunction. However, the underlying mechanisms behind these impairments are not clear. Here, we utilized BTBR T + Itpr tf /J (BTBR) mice, an animal model of autism, to investigate the involvement of abnormal cerebellar development in motor performance. We found BTBR mice exhibited severe dystonia-like behavior and motor coordination or motor learning impairments. The onset of these abnormal movements coincided with the increased proliferation of granule neurons and enhanced foliation, and Purkinje cells displayed morphological hypotrophy with increased dendritic spine formation but suppressed maturation. The migration of granule neurons seemed unaffected. Transcriptional analyses confirmed the differential expression of genes involved in abnormal neurogenesis and revealed TRPC as a critical regulator in proliferation and synaptic formation. Taken together, these findings indicate that abnormal cerebellar development is closely related to dystonia-like behavior and motor dysfunction of BTBR mice and that TRPC may be a novel risk gene for ASD that may participate in the pathological process of autistic movement disorders.

The hydrogenation of nitrogen‐containing heterocyclic precursors in aqueous medium is quite challenging, especially at low temperature and without imposing molecular hydrogen pressure. In the light of the edges of metal nanoparticles (NPs) possess high selective activity, but most of the exposed metal surface does not. Hence, to influence the activity of the entire NPs surface, the use of zeolitic imidazolate frameworks (ZIFs) to obtain the metal NPs encapsulated in the carbon tubes which has been applied frequently. Herein, we design and synthesize a series of metal catalysts encapsulated in N‐doped carbon nanotubes (NCT), which disperse on the hollow N‐doped carbon framework (HNC), via pyrolysis ZIF‐67, ZIF‐67@ZIF‐8, and ZIF‐8@ZIF‐67 step by step. The catalyst of Co@NCT/HNC shows outstanding activity of hydrogenation of quinoline under mild conditions, due to the synergistic effects between Co NPs, NCT and HNC, such as the NCT make the hydrogen reach the surface of the reactant rapidly, and the encapsulated structure can enormously prevent the metal aggregating.

Background Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impairments in social interactions and communication and stereotypical patterns of behaviors, interests, or activities. Even with the increased prevalence of ASD, there is no defined standard drug treatment for ASD patients. Currently, stem cells, including human amniotic epithelial cell (hAEC) transplantation, seem to be a promising treatment for ASD, but the effectiveness needs to be verified, and the mechanism has not been clarified. Methods We intraventricularly transplanted hAECs into a 2-month-old BTBR T+tf/J (BTBR) mouse model of ASD. Behavior tests were detected 1 month later; hippocampal neurogenesis, neuroprogenitor cell (NPC) pool, and microglia activation were analyzed with immunohistochemistry and immunofluorescence; the levels of pro-inflammatory cytokines, brain-derived neurotrophic factor (BDNF), and TrkB in the hippocampus were determined by real-time PCR or western blotting. Results After intraventricular injection of hAECs into adult males, social deficits in BTBR mice were significantly ameliorated. In addition, hAEC transplantation restored the decline of neurogenesis and NPCs in the hippocampus of BTBR mice by expanding the stem cell pool, and the decreased levels of BDNF and TrkB were also rescued in the hippocampus of the hAEC-injected BTBR mice. Meanwhile, the transplantation of hAECs did not induce microglial overactivation or excessive production of pro-inflammatory cytokines in the hippocampus of BTBR mice. Conclusions Based on these results, we found that hAEC transplantation ameliorated social deficits and promoted hippocampal neurogenesis in BTBR mice. Our study indicates a promising therapeutic option that could be applied to ASD patients in the future.

Gut microbiota and childhood maltreatment are closely related to depressive symptoms. This study aimed to analyze the characteristics of gut microbiota in major depressive disorder (MDD) patients with childhood maltreatment experience and explore the correlation between gut microbiota, childhood maltreatment, and depressive symptoms. A total of 37 healthy controls (HCs) and 53 patients with MDD were enrolled, including 18 MDD patients without childhood maltreatment experience and 35 MDD patients with childhood maltreatment experience. The Hamilton’s Depression Scale (HAMD-24) and Childhood Trauma Questionnaire-Short Form (CTQ-SF) were used to evaluate their depressive symptoms and childhood maltreatment experience, respectively. The composition of gut microbiota was evaluated using 16S rRNA sequencing. Spearman’s correlation analysis was used to evaluate the correlation between different gut microbiota, depressive symptoms and childhood maltreatment. The mediation analysis was used to evaluate the mediating effect of gut microbiota. In the α-diversity analysis, we found that the Simpson index and Pielou’s Evenness index differed significantly between MDD patients without childhood maltreatment experience and HCs. In the β-diversity analysis, principal coordinate analysis (PCoA) showed significant differences between MDD patients without childhood maltreatment experience, MDD patients with childhood maltreatment experience and HCs. Twenty-seven different bacteria were identified through Linear discriminant analysis effect size (LEfSe) analysis at different levels of classification. The analysis of the correlation showed that Blautia, Bifidobacterium, Bacteroides, Roseburia, and Phascolarctobacterium were significantly correlated with HAMD and CTQ-SF scores. The mediation analysis showed that childhood maltreatment had a significant direct effect on the patients’ depressive symptoms, and Blautia, Bifidobacterium, Roseburia had a significant mediating effect. The findings of this study suggested that MDD patients with childhood maltreatment experience had different gut microbiota, which might have a mediating effect on the influence of childhood maltreatment on depressive symptoms.