Traditionally, Asian ginseng or Korean ginseng, Pana x ginseng has long been used in Korea and China to treat various diseases. The main active components of Panax ginseng is ginsenoside, which is known to have various pharmacological treatment effects such as antioxidant, vascular easing, anti-allergic, anti-inflammatory, anti-diabetes, and anticancer. Most reactive oxygen species (ROS) cause chronic diseases such as myocardial symptoms and cause fatal oxidative damage to cell membrane lipids and proteins. Therefore, many studies that inhibit the production of oxidative stress have been conducted in various fields of physiology, pathophysiology, medicine and health, and disease. Recently, ginseng or ginsenosides have been known to act as antioxidants in vitro and in vivo results, which have a beneficial effect on preventing cardiovascular disease. The current review aims to provide mechanisms and inform precious information on the effects of ginseng and ginsenosides on the prevention of oxidative stress and cardiovascular disease in animals and clinical trials.

Based on the quinazoline bearing EGFR inhibitors, a series of thirty four compounds having a quinoline scaffold were synthesized and evaluated in vitro for EGFR kinase inhibitory and anticancer activities.

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Disruption of Pseudomonas putida KT2440 by ultrasound treatment in a bath sonicator, in presence of the glass beads, was carried out for the release of arginine deiminase (ADI) and the results were compared with that of by Dyno-mill. The release of ADI depended mainly on the bead size and cellmass concentration being disrupted in bead mill. Nearly 23 U mL ADI was released when slurry with a cell-mass concentration of 250 g L was disintegrated for 9 min with 80% bead loading (0.25 mm) in Dyno-mill. Marginally higher amount of ADI (24.1 U mL ) was released by the bath sonication of 250 g L cellmass slurry for 30 min with the beads (0.1 mm) and a sonication power of 170 W. The glass beads, suspended along with the cellmass slurry in bath sonicator, efficiently disrupted the microbial cells to release ADI. Variation in the kinetic constants for the performance parameters implied that ADI release and cell disruption kinetics is a function of disruption technique used and the process variables thereof. Estimation of location factor suggested that selective release of ADI can be achieved. © 2018 American Institute of Chemical Engineers Biotechnol. Prog., 2018 © 2018 American Institute of Chemical Engineers Biotechnol. Prog., 34:1185-1194, 2018.