Formation mechanism of iron-catechol complexes in the colored periostracum of Corbicula spp.

The shell color of Corbicula clams, which are globally distributed, is roughly divided into yellowish and blackish depending on the environmental conditions of the sediment. The formation of an iron-L-3,4-dihydroxyphenylalanine (DOPA) complex in a thin organic layer, called the periostracum, on a calcareous layer causes the blackening of the clamshell. However, the iron-DOPA complex formation mechanism is unclear.

A Self-Emulsified Adjuvant System Containing the Immune Potentiator Alpha Tocopherol Induces Higher Neutralizing Antibody Responses than a Squalene-Only Emulsion When Evaluated with a Recombinant Cytomegalovirus (CMV) Pentamer Antigen in Mice.

The development of new vaccine adjuvants represents a key approach to improvingi the immune responses to recombinant vaccine antigens. Emulsion adjuvants, such as AS03 and MF59, in combination with influenza vaccines, have allowed antigen dose sparing, greater breadth of responses and fewer immunizations. It has been demonstrated previously that emulsion adjuvants can be prepared using a simple, low-shear process of self-emulsification (SE).

ALKBH5-mediated mA mRNA methylation governs human embryonic stem cell cardiac commitment.

N6-methyladenosine (mA), as the most abundant modification of mammalian messenger RNAs, is essential for tissue development and pathogenesis. However, the biological significance of mA methylation in cardiac differentiation and development remains largely unknown. Here, we identify that the downregulation of mA demethylase ALKBH5 is responsible for the increase of mA methylation and cardiomyocyte fate determination of human embryonic stem cells (hESCs) from mesoderm cells (MESs).

Loss of mA methyltransferase METTL3 promotes heart regeneration and repair after myocardial injury.

Aims: N6-Methyladenosine (mA), one of the important epigenitic modifications, is very commom in messenger RNAs (mRNAs) of eukaryotes, and has been involved in various diseases. However, the role of mA modification in heart regeneration after injury remains unclear. The study was conducted to investigate whether targeting methyltransferase-like 3 (METTL3) could replenish the loss of cardiomyocytes (CMs) and improve cardiac function after myocardial infarction (MI).