Research progress on the modulation mechanism of electroacupuncture for learning and memory impairment after ischemic stroke / 中国针灸

Electroacupuncture may play a role in treatment of learning and memory impairment after ischemic stroke by regulating phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt) signaling pathway, cyclic adenosine monophosphate (cAMP)-dependent protein kinase A (PKA)/cAMP response element binding protein (CREB) signaling pathway, nerve growth factor (NGF)/tyrosine kinase-A (TrkA) signaling pathway, Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway, Notch signaling pathway, erythropoietin-producing hepatocyte (Eph)/ephrin signaling pathway. The interactions among these pathways should be further explored in treatment of learning and memory impairment after ischemic stroke.

Expression of Cyclin D1 in wound healing of human corneal epithelial cells with high blood glucose level / 国际眼科杂志(Guoji Yanke Zazhi)

@#AIM: To study the effect of high glucose environment on human corneal epithelial cell injury and repair, and to explain the significance of Cyclin D1 protein expression in corneal epithelial cell wound healing in high glucose culture. <p>METHODS: The high-glucose micro-environment of diabetic corneal lesions was simulated. After human corneal epithelial cells were resuscitated, cultured and passaged, a normal control group of DMEM complete medium of equal volume of distilled water and a high-glucose treated group of DMEM complete medium containing 25mmol/L glucose were set respectively. After the cells were overgrown, the cells were stimulated with scratches. The growth conditions and changes of the cells in each group were observed and compared under an inverted phase contrast microscope. Western glucose was used to analyze high glucose at different time points(0, 12, 24, 48, and 72h)Cyclin D1 Protein expression in cultured corneal epithelial cells. The qRT-PCR was used to analyze high glucose at different time points and each group Cyclin D1 mRNA expression.<p>RESULTS: Under the conditions of high glucose treatment <i>in vitro</i>, the repair rate of human corneal epithelial cells was slowed down after injury, floating cells increased, cells reattached less, and cell spacing increased. With the increase of high glucose treatment time, the cell state became worse and the growth rate slow; normal group repaired cell damage faster, increased cell density, regular morphology, and smooth cell membrane. Cyclin D1 expression was up-regulated by Western blot, but the up-regulation effect gradually weakened with time. The highest expression of Cyclin D1 in both groups appeared at 12h. The expression of Cyclin D1 in the high glucose treatment group was lower than that in the normal control group. The qRT-PCR results showed that after high glucose treatment, the expression of Cyclin D1 mRNA was up-regulated, but with the increase of high glucose treatment time, the up-regulation effect weakened, and the mRNA level recovered to the same level as the control group at 48h. <p>CONCLUSION: In the process of corneal epithelial cell wound healing, high glucose negatively regulates and inhibits the expression of Cyclin D1 protein, and is related to the decline of corneal epithelial cell proliferation and apoptosis.

A novel mutation in the ETFDH gene of an infant with multiple acyl-CoA dehydrogenase deficiency / 中国当代儿科杂志

This article reports the results of tandem mass spectrometry and the mutation features of the ETFDH gene for an infant with multiple acyl-CoA dehydrogenase deficiency. The results of tandem mass spectrometry showed that C14 : 1, C8, C6, C10, and C12 increased. Exon sequencing was performed on this infant and his parents and revealed double heterozygous mutations in the ETFDH gene of the infant: c.992A>T and c.1450T>C. The former was inherited from his mother, and the latter was inherited from his father. c.1450T>C was shown to be the pathogenic mutation in the HGMD database. PolyPhen2, SIFT, and PROVEAN all predicted that the novel mutation c.992A>T might be pathogenic, and the mutant amino acids were highly conserved across various species. The findings expand the mutation spectrum of the ETFDH gene, and provide molecular evidence for the etiological diagnosis of the patient with multiple acyl-CoA dehydrogenase deficiency as well as for the genetic counseling and prenatal diagnosis in the family.