The ubiquitin-editing enzyme TNFAIP3 exerts neuroprotective roles in epilepsy rats through repressing inflammation.

The ubiquitin-editing enzyme TNF alpha-induced protein 3 (TNFAIP3) emerges protective roles in neurological disorder, such as cerebral trauma. However, the molecular mechanisms of TNFAIP3 in epilepsy are not very clear. Hereon, the epileptic mouse models and BV2 microglial cellular models were established by kainic acid (KA) and lipopolysaccharide (LPS) respectively.

A Retrospective Study on Clinical Features of Childhood Moyamoya Disease.

Background: Childhood moyamoya disease (MMD) can lead to progressive and irreversible neurological impairment. Early age at onset is likely associated with a worst prognosis of the disease. The study aims to summarize the clinical characteristics of childhood MMD for supporting the diagnosis and treatment of early MMD.

Ginsenoside Rb1 Alleviates Lipopolysaccharide-Induced Inflammatory Injury by Downregulating miR-222 in WI-38 Cells.

Pneumonia is a serious respiratory tract infection disease in children, which threatens to the health or life of children patients. Ginsenoside Rb1 (Rb1) is a principle active ingredient extracted from the root of F.H.

[Identification of pathogenic mutation in a Chinese pedigree affected with split hand/split foot malformation].

Objective: To detect potential mutation in a Chinese pedigree affected with split hand/split foot malformation (SHFM).

Methods: The patients were screened for genome-wide copy number variations with single nucleotide polymorphism (SNP) microarray. Copy number variations were verified by real-time fluorescence quantitative PCR.

Selective targeting of MAPK family kinases JNK over p38 by rationally designed peptides as potential therapeutics for neurological disorders and epilepsy.

Human mitogen-activated protein kinase (MAPK) family members JNK and p38 are two homologous protein-serine/threonine kinases but play distinct roles in the pathological process of neurological disorders. Selective targeting of JNK over p38 has been established as a potential therapeutic approach to epilepsy and other nervous system diseases. Herein, we describe an integrated in vitro-in silico protocol to rationally design kinase-peptide interaction specificity based on crystal structure data.

A case of late-onset riboflavin responsive multiple acyl-CoA dehydrogenase deficiency (MADD) with a novel mutation in ETFDH gene.

We report a novel mutation in the electron transfer flavoprotein dehydrogenase (EFTDH) gene in an adolescent Chinese patient with late-onset riboflavin-responsive multiple acyl-CoA dehydrogenase deficiency (MADD) characterized by muscle weakness as early symptom. At the age of 9 years, the patient experienced progressive muscle weakness. Blood creatine kinase level and aminotransferase were higher than normal.

Mycoplasma pneumonia combined with pulmonary infarction in a child.

We reported a 9-year-old boy with mycoplasma pneumonia who developed pulmonary infarction. The child first had fever and cough, and then had difficult breathing. But, the signs of his lung were not obvious.