Alkenyl Succinic Anhydride (ASA) is a sizing agent used in papermaking to increase the water repellency of paper. Almost 60 years after the introduction of the chemical in papermaking, scientists still have differing views on how ASA interacts with cellulose. Several experiments were conducted to bring more clarity to the ASA sizing mechanism, especially on the contentious question of ASA-cellulose covalent bonding or the esterification reaction between ASA and cellulose during papermaking. Herein, research papers and patents, including experiments and results, from the1960’s to 2020 were reviewed. Our investigation revealed that the ester bond formation between ASA and cellulose is insignificant and is not a prerequisite for sizing effectiveness; the main ASA related material found in sized paper is hydrolyzed ASA or both hydrolyzed ASA and ASA salt. In addition, ASA emulsion stability and ASA emulsion retention are important for sizing efficiency improvement.

Maternal hyperglycemia, induced by gestational diabetes mellitus (GDM), has detrimental effects on fetal vascular development, ultimately increasing the risk of cardiovascular diseases in offspring. The potential underlying mechanisms by which these complications occur are through functional impairment and epigenetic changes in fetal endothelial progenitor cells (EPCs), however, remain less defined. We confirm that intrauterine hyperglycemia leads to impaired angiogenic function of fetal EPCs, as observed through functional assays of outgrowth endothelial cells (OECs) derived from fetal EPCs of GDM pregnancies (GDM-EPCs). Notably, PCDH10 expression is increased in OECs derived from GDM-EPCs, which is associated with the inhibition of angiogenic function in fetal EPCs. Additionally, increased PCDH10 expression is correlated with hypomethylation of the PCDH10 promoter. Our findings demonstrate that in utero exposure to GDM can induce angiogenic dysfunction in fetal EPCs through altered gene expression and epigenetic changes, consequently increasing the susceptibility to cardiovascular diseases in offspring of GDM mothers.

Osteoporosis, often linked to increased osteoclast activity due to menopause or aging, was the focus. In this study, the inhibitory effects of Salicornia europaea L. (SE) water extract of desalted SE (WSE) were investigated on osteoclast differentiation and bone loss in ovariectomized mice. The findings revealed that WSE effectively inhibited RANKL-induced osteoclast differentiation, as evidenced by TRAP staining, and also suppressed bone resorption and F-actin ring formation in a dose-dependent manner. Gene expressions related to osteoclast differentiation, including NFATc1, TRAP, cathepsin K, and DC-STAMP, were downregulated by WSE. Oral administration of WSE improved bone density and structural parameters in ovariectomized mice. Dicaffeoyl quinic acids (DCQAs) and saponins in WSE were detected, with 3,4-, 3,5-, and 4,5-DCQA isolated and identified. All tested DCQAs, including the aforementioned types, inhibited osteoclast differentiation, bone resorption, and the expression of osteoclast-related genes. Furthermore, WSE and DCQAs reduced ROS production mediated by RANKL. These results indicate the potential of WSE and its components, DCQA, as preventive or therapeutic agents against osteoporosis and related conditions.