Dysfunction in social interactions is a core symptom of autism spectrum disorder (ASD). Nevertheless, the neural mechanisms underlying social deficits in ASD are poorly understood. By integrating electrophysiological, in vivo fiber photometry, viral-mediated tracing, optogenetic and pharmacological stimulation, we show reduced intrinsic excitability and hypoactivity of SOM interneurons in medial prefrontal cortex (mPFC) in Magel2-deficient mice, an established ASD model, were required to social defects.
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February 2025
Dimethyl phthalate (DMP) has been extensively utilized as a plasticizer on a global scale for many years. Its presence in the environment and its harmful effects on living organisms have raised concerns. This study aimed to examine its potential developmental neurotoxicity by utilizing zebrafish as a model.
View Article and Find Full Text PDFBisphenol A (BPA) is a widespread environmental endocrine disruptor (EED) that can cause various environmental and health issues by inducing oxidative stress. The c-Jun N-terminal kinase (JNK) signaling pathway plays a crucial role in oxidative stress-mediated cellular damage. Although folic acid (FA) has demonstrated antioxidant properties, its potential protective effects against BPA-induced developmental and neurotoxicity, as well as the mechanisms involved in the JNK signaling pathway, are still not completely understood.
View Article and Find Full Text PDFBackground: Paediatric professional scarcity and uneven distribution is acute in underdeveloped regions, exacerbated by COVID-19's workload surge and burnout, highlighting the need for strengthened prevention and response measures.
Aim: Propose an effective talent management model to address the challenge of paediatric medical personnel shortage and lack of management experience in Underdeveloped cities of developing countries.
Methods: A crisis management plan has been implemented in a paediatric hospital in Henan, China, with a talent framework to ensure a skilled, stable workforce.
Pin1 is a unique isomerase that regulates protein conformation and function after phosphorylation. Pin1 aberration contributes to some neurological diseases, notably Alzheimer's disease, but its role in epilepsy is not fully understood. We found that Pin1-deficient mice had significantly increased seizure susceptibility in multiple chemical inducing models and developed age-dependent spontaneous epilepsy.
View Article and Find Full Text PDFHepatocellular carcinoma (HCC) is the second leading cause of cancer related-death. As a major common regulator of numerous cancer-driving pathways and a unique therapeutic target, the prolyl isomerase Pin1 is overexpressed in a majority of HCCs, whereas the mechanism underlying Pin1 overexpression remains elusive. Here we find that miR-140-5p inhibits HCC by directly targeting Pin1 to block multiple cancer-driving pathways.
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