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The impact of pulsed laser radiation on carbon nanotube growth and structure has attracted considerable interest because of the potential application of CNTs as composite materials for advanced materials. In this work we study the influence of laser parameters on CNT’s exposed to nanosecond laser pulses, using femtosecond IR radiation to temporally separate the nanosecond pulse propagation time from the subsequent laser-induced structural changes. The system is operated in a liquid helium cold-finger environment and the laser-induced structural changes are recorded in situ by IR spectroscopy. We measure the optical loss at fundamental and second-harmonic wavelengths induced by the laser fluence and find that the fluence threshold for optical damage is lower than that for laser ablation or re-growth. The intensity threshold for photo-induced defects formation is also relatively low, and below the intensity level at which carbon ablation is observed.Mitochondrial complex I deficiency causes severe neurodegenerative disease in mice.
Major neurodegenerative diseases are often linked with energy metabolism dysfunction. A possible link between neurodegeneration and mitochondrial functions is encoded by the Apoptosis-Inducing Factor (AIF), a caspase-independent cell death executioner. AIF is controlled by the Bcl-2 family of proteins and is released from mitochondria under Ca2+-independent and caspase-independent processes. Its release is stimulated by mitochondrial complex I inhibition in cultured cells. In this report, we investigated the implications of AIF release after mitochondrial complex I inhibition by α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) in neurons. In wild-type mice, AMPA induced Ca2+-independent AIF release from mitochondria, and AIF translocation to the nucleus after AMPA washout. This process was associated with an increase in the number of histone H3-T145 phosphorylated (phospho) centromere protein-B (CENP-B) foci. Moreover, we show that neurons from Complex I-deficient mutant mice, generated by heterozygous knockout of the nuclear-encoded ndufs4 subunit of
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