Mitochondrial respiratory quiescence: A new model for examining the role of mitochondrial metabolism in development.

Mitochondria are vital organelles with a central role in all aspects of cellular metabolism. As a means to support the ever-changing demands of the cell, mitochondria produce energy, drive biosynthetic processes, maintain redox homeostasis, and function as a hub for cell signaling. While mitochondria have been widely studied for their role in disease and metabolic dysfunction, this organelle has a continually evolving role in the regulation of development, wound repair, and regeneration.

Heritable shifts in redox metabolites during mitochondrial quiescence reprogramme progeny metabolism.

Changes in maternal diet and metabolic defects in mothers can profoundly affect health and disease in their progeny. However, the biochemical mechanisms that induce the initial reprogramming events at the cellular level have remained largely unknown owing to limitations in obtaining pure populations of quiescent oocytes. Here, we show that the precocious onset of mitochondrial respiratory quiescence causes a reprogramming of progeny metabolic state.

Growth inhibitory activity of Ankaferd hemostat on primary melanoma cells and cell lines.

Objective: Ankaferd hemostat is the first topical hemostatic agent about the red blood cell-fibrinogen relations tested in the clinical trials. Ankaferd hemostat consists of standardized plant extracts including , and . The aim of this study was to determine the effect of Ankaferd hemostat on viability of melanoma cell lines.