The present study aimed to investigate the composition and potential anticancer activities of essential oils obtained from two species, myrrh and frankincense, by hydrodistillation. Using gas chromatography-mass spectrometry (GC-MS), 76 and 99 components were identified in the myrrh and frankincense essential oils, respectively, with the most abundant components, 2-Cyclohexen-1-one, 4-ethynyl-4-hydroxy-3,5,5-trimethyl- and n-Octylacetate, accounting for 12.01 and 34.66%, respectively. The effects of the two essential oils, independently and as a mixture, on five tumor cell lines, MCF-7, HS-1, HepG2, HeLa and A549, were investigated using the MTT assay. The results indicated that the MCF-7 and HS-1 cell lines showed increased sensitivity to the myrrh and frankincense essential oils compared with the remaining cell lines. In addition, the anticancer effects of myrrh were markedly increased compared with those of frankincense, however, no significant synergistic effects were identified. The flow cytometry results indicated that apoptosis may be a major contributor to the biological efficacy of MCF-7 cells.

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Gamma glutamyl cysteine ligase (GCL) is the rate-limiting enzyme for intracellular glutathione (GSH) synthesis. The GSH concentration and GCL activity are declining with age in the central nervous system (CNS), and is accompanied by elevated reactive oxygen species (ROS). To study the biological effects of low GSH levels, we disrupted its synthesis both at birth by breeding a Gclc loxP mouse with a thy1-cre mouse (NEGSKO mouse) and at a later age by breeding with a CaMKII-ERT2-Cre (FIGSKO mouse). NEGSKO mice with deficiency of the Gclc in their entire CNS neuronal cells develop at 4 weeks: progressive motor neuron loss, gait problems, muscle denervation and atrophy, paralysis, and have diminished life expectancy. The observed neurodegeneration in Gclc deficiency is of more chronic rather than acute nature as demonstrated by Gclc targeted single-neuron labeling from the inducible Cre-mediated knockout (SLICK) mice. FIGSKO mice with inducible Gclc deficiency in the forebrain at 23 weeks after tamoxifen induction demonstrate profound brain atrophy, elevated astrogliosis and neurodegeneration, particularly in the hippocampus region. FIGSKO mice also develop cognitive abnormalities, i.e. learning impairment and nesting behaviors based on passive avoidance, T-Maze, and nesting behavior tests. Mechanistic studies show that impaired mitochondrial glutathione homeostasis and subsequent mitochondrial dysfunction are responsible for neuronal cell loss. This was confirmed by mitochondrial electron transporter chain activity analysis and transmission electron microscopy that demonstrate remarkable impairment of state 3 respiratory activity, impaired complex IV function, and mitochondrial swollen morphology in the hippocampus and cerebral cortex. These mouse genetic tools of oxidative stress open new insights into potential pharmacological control of apoptotic signaling pathways triggered by mitochondrial dysfunction.

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In this paper, a universal adaptive driving scheme for synchronous rectification (SR) is proposed. The drain to source voltage of the synchronous rectifier is sensed so that the paralleled body diode conduction is detected. Using the proposed SR driving scheme, the SR turn-OFF time is tuned to eliminate the body diode conduction. The SR gate driving signal can be tuned within all operating frequency regions. Moreover, a simple digital implementation is introduced. Compared with analog ones, it enables more intelligent and precise SR control, improving converter efficiency. For rapid prototyping purposes, the digital SR tuning system is realized in Cyclone III field-programmable gate array (FPGA)

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