Multiplexing of TMT labeling reveals folate-deficient diet-specific proteome changes in NTDs.

In the early stage of embryonic development, the neural tube (NT) cannot be closed properly due to some complex factors, including environmental factors, genetic factors, and the relationship between various factors, leading to the occurrence of neural tube defects (NTDs). In this study, we induced a mouse model of NTDs by feeding mice with a low-folate diet and intraperitoneally injecting them with 1.5 mg/kg methotrexate on E7.

Acetylome analyses provide novel insights into the effects of chronic intermittent hypoxia on hippocampus-dependent cognitive impairment.

Introduction: Chronic intermittent hypoxia (CIH) can negatively affect hippocampal function through various molecular mechanisms. Protein acetylation, a frequently occurring modification, plays crucial roles in synaptic plasticity and cognitive processes. However, the global protein acetylation induced by CIH in the hippocampus and its specific effects on hippocampal function and behavior remain poorly understood.

Intergenerational association of gut microbiota and metabolism with perinatal folate metabolism and neural tube defects.

Disorders of folic acid metabolism during pregnancy lead to fetal neural tube defects (NTDs). However, the mechanisms still require further investigation. Here, we aim to analyze the brain metabolic profiles of 30 NTDs and 30 healthy fetuses.

N6-methyladenosine participates in mouse hippocampus neurodegeneration via PD-1/PD-L1 pathway.

Developmental abnormalities and hippocampal aging leads to alteration in cognition. In the brain, N6-methyladenosine (mA) is a common and reversible mRNA alteration that is essential for both neurodevelopment and neurodegeneration. However, its function in the postnatal hippocampus and the specific mechanisms regulating hippocampus-related neurodegeneration still awaits elucidate.

Folate-deficiency induced acyl-CoA synthetase short-chain family member 2 increases lysine crotonylome involved in neural tube defects.

Maternal folate deficiency increases the risk of neural tube defects (NTDs), but the mechanism remains unclear. Here, we established a mouse model of NTDs low folate diets combined with MTX-induced conditions. We found that a significant increase in butyrate acid was observed in mouse NTDs brains.

Sodium butyrate mediates histone crotonylation and alleviated neonatal rats hypoxic-ischemic brain injury through gut-brain axis.

Neonatal hypoxic-ischemic encephalopathy (HIE) refers to nervous system damage caused by perinatal hypoxia, which is the major cause of long-term neuro-developmental disorders in surviving infants. However, the mechanisms still require further investigation. In this study, we found that the butanoate metabolism pathway exhibited significantly decreased and short chain fatty acid (SCFAs)-producing bacteria, especially butyrate-producing bacteria, were significantly decreased in fecal of neonatal hypoxic-ischemic brain damage (HIBD) rats.

Abnormal transcriptome-wide DNA demethylation induced by folate deficiency causes neural tube defects.

Neural tube defect (NTDs) is one of the most common and serious fetal and neonatal birth defects. Neural tube closure (NTC) is an exquisitely coordinated process and this procedure is influenced by both genetic and environmental factor. Folic acid (FA) supplementation is an effective for prevention of a proportion of NTDs, however, the mechanism remains unclear.

Transcriptome Analyses of Senecavirus A-Infected PK-15 Cells: RIG-I and IRF7 Are the Important Factors in Inducing Type III Interferons.

Senecavirus A (SVA) is a new type of virus related to swine vesicular disease, which results in enormous economic losses worldwide. At present, the host transcriptional responses to SVA infection, host-SVA interactions, and the mechanism of SVA in innate immune modulation are not well understood. This study explores the gene expression profiles of PK-15 cells at 0, 6, 12, 18, 24, 36 h SVA post-infection by RNA sequencing.

Genetic variations in S gene of porcine epidemic diarrhoea virus from 2018 in Sichuan Province, China.

Porcine epidemic diarrhoea virus (PEDV) belongs to the family Coronavirus, a genus of coronavirus, a highly contact-infectious intestinal disease pathogen. In this study, we downloaded 62 PEDV S gene sequences uploaded to GenBank, including 10 uploaded by our laboratory from 2018, and constructed a PEDV S gene evolution tree using MEGA V7.0 software.