<span style="font-size: 21.0pt;mso-bidi-font-size:14.0pt;font-family:"Times New Roman","serif"">Effect of <i><span style="font-size:21.5pt;mso-bidi-font-size:14.5pt; font-family:"Times New Roman","serif"">Semecarpus anacardium </span></i><span style="font-size:21.0pt;mso-bidi-font-size:14.0pt;font-family:"Times New Roman","serif"">nuts on lipid peroxidation </span></span>

798-801<span style="font-size: 16.0pt;mso-bidi-font-size:9.0pt;font-family:" times="" new="" roman","serif""="">Alcoholic extract of pericarp showed significant protection against FeSO4 induced lipid peroxidation, as compared with whole native nut and seeds. Mechanism of action may be through metal chelation or activation of endogenous antioxidant enzymes, because the ex tract did not show hydroxyl and super oxide anion scavenging property. Further <span style="font-size:15.5pt; mso-bidi-font-size:8.5pt;font-family:" times="" new="" roman","serif""="">in vitro experiments against FeSO4 ,it did not maintain the level of reduced glutathione. </span

A novel vascular disrupting agent plinabulin triggers JNK-mediated apoptosis and inhibits angiogenesis in multiple myeloma cells

Previous studies have established a role of vascular-disrupting agents as anti- cancer agents. Plinabulin is a novel vascular-disrupting agent that exhibits potent interruption of tumor blood flow because of the disruption of tumor vascular endothelial cells, resulting in tumor necrosis. In addition, plinabulin exerts a direct action on tumor cells, resulting in apoptosis. In the present study, we examined the anti–multiple myeloma (MM) activity of plinabulin. We show that low concentrations of plinabulin exhibit a potent antiangiogenic action on vascular endothelial cells. Importantly, plinabulin also induces apoptotic cell death in MM cell lines and tumor cells from patients with MM, associated with mitotic growth arrest. Plinabulin-induced apoptosis is mediated through activation of caspase-3, caspase-8, caspase-9, and poly(ADP-ribose) polymerase cleavage. Moreover, plinabulin triggered phosphorylation of stress response protein JNK, as a primary target, whereas blockade of JNK with a biochemical inhibitor or small interfering RNA strategy abrogated plinabulin-induced mitotic block or MM cell death. Finally, in vivo studies show that plinabulin was well tolerated and significantly inhibited tumor growth and prolonged survival in a human MM.1S plasmacytoma murine xenograft model. Our study therefore provides the rationale for clinical evaluation of plinabulin to improve patient outcome in MM

Abstracts of the International Chemical Engineering Conference 2021: 100 Glorious Years of Chemical Engineering & Technology

This book presents the selected abstracts of the International Chemical Engineering Conference 2021, hosted from the 16th to 19th of September 2021 in virtual mode by the Department of Chemical Engineering, NIT Jalandhar, India. Conference Title: International Chemical Engineering Conference 2021Conference Acronym: ICheEC2021Theme: 100 Glorious Years of Chemical Engineering &amp; TechnologyConference Date: 16-19 September 2021Conference Location: OnlineConference Organizer: Department of Chemical Engineering, NIT Jalandhar, Indi