An Ultimate Question for Functional A-to-I mRNA Editing: Why Not a Genomic G?

A-to-I mRNA editing resembles A-to-G mutations. Functional mRNA editing, representing only a corner of total editing events, can be inferred from the experimental removal of editing. However, it is intuitive to ask why evolution chose RNA editing rather than directly (and simply) changing the genomic sequence to G? If G is better than A, then drift or constructive neutral evolution (CNE) theory can explain the emergence of such editing, but it is still unclear why the exemplified conserved editing is perfectly maintained without observing any subsequent A-to-G DNA mutations? Virtually every functional and conserved mRNA editing site faces this ultimate question until one justifies that being editable is better than a hardwired genomic allele.

Celastrol Treatment Ameliorated Acute Ischemic Stroke-Induced Brain Injury by Microglial Injury Inhibition and Nrf2/HO-1 Pathway Activations.

Background: Stroke is the third main reason of mortality, which is the leading reason for adult disability in the globe. Poststroke inflammation is well known to cause acute ischemic stroke- (AIS-) induced brain injury (BI) exacerbation. Celastrol (CL) has exhibited anti-inflammatory activities in various inflammatory traits though underlying mechanisms remain unknown.

Exosome circRNAs and ceRNA network profiles in different ANA sera.

Increasing evidences show that circRNAs are associated with some autoimmunity diseases either as a biomarker or therapeutic target. Exosomes containing nucleic acids and proteins are found in sera of series diseases and could serve as either diagnostic or therapeutic target. ANA serves as first common diagnostic test for autoimmunity disease, different ANA staining reflecting different types of autoimmunity disease.

Clinical significance of 5-(and 6)-carboxyfluorescein diacetate succinimidyl ester-labeled microspheres for detecting endothelial progenitor cells in human peripheral blood.

The aims of the present study were to establish a single-platform flow cytometry method using 5-(and 6)-carboxyfluorescein diacetate succinimidyl ester (CFSE)-labeled microspheres as the reference for determining endothelial progenitor cell (EPC) number and to evaluate the efficacy of this detection method. Single-platform flow cytometry was used to count cell numbers using CFSE-stained fluorescent microspheres as the internal reference and the EPC numbers in specimens using this novel method were compared with an clonogenic counting assay. The results of the two counting methods were consistent and compared with the clonogenic counting assay, the time and cost of the novel method was markedly reduced, as were the corresponding technical requirements.

A novel somatic MAPK1 mutation in primary ovarian mixed germ cell tumors.

A recent exome-sequencing study revealed prevalent mitogen-activated protein kinase 1 (MAPK1) p.E322K mutation in cervical carcinoma. It remains largely unknown whether ovarian carcinomas also harbor MAPK1 mutations.

GM-CSF induces cyclin D1 expression and proliferation of endothelial progenitor cells via PI3K and MAPK signaling.

Background/aims: Endothelial progenitor cells (EPCs), which can be isolated from the bone marrow or the peripheral blood, have generated interest because of their capacity to migrate to sites of vascularization and endothelialization and differentiate into endothelial cells in a process termed neovasculogenesis. EPCs are therefore possible regenerative tools for the treatment of vascular diseases and potential targets for the inhibition of angiogenesis during tumor development. Here, we investigated the mechanisms underlying the effect of granulocyte-macrophage colony-stimulating factor (GM-CSF) on the acceleration of EPC proliferation and colony formation.

Th17-relevant cytokines vary with sera of different ANA staining patterns.

Antinuclear antibodies (ANA) react with components located in the cell nucleus and cytoplasm. Differing ANA staining patterns may reflect the specificity of autoantibodies in sera and indicate some autoimmune diseases specifically, to some extent. Th17-relevant cytokines have been shown to be involved in a variety of autoimmune diseases, but not consistently.