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The thickness dependent chain mobility in polymer films influenced by the interfacial effect was investigated by the cold crystallization behavior of thin poly­(ethylene terephthalate) (PET) films covered by a thin poly­(2,6-dimethyl-1,4-phenyleneoxide) (PPO) layer to eliminate the free surface effect. Two characteristic film thicknesses were observed, which were related to the long-range perturbations of the interfacial effect. Below the first thickness (h s*), the bulk-like crystallization temperature of PET films begins to shift upward, and below the second thickness (h n*), crystallization of PET films is completely suppressed. These two characteristic thicknesses are proportional to the adsorbed layer thickness. We found that h s* is much greater than the thickness of the PET film with a free surface, while h n* is independent of the free surface. This result indicated that the thickness for the suppression of polymer film dynamics can be increased by removing the contribution of the free surface. The value of h n * independent of the free surface may be attributed to the fact that the chain conformation within this thickness adopts the chain conformation at the interface, causing the “free surface” to vanish. The chain conformations affected by the substrate are another cause of long-range perturbations.

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Mitochondria are the energy production center in cells, which regulate aerobic metabolism, calcium balance, gene expression and cell death. Their homeostasis is crucial for cell viability. Although mitochondria own a nucleus-independent and self-replicating genome, most of the proteins, which fulfill mitochondrial functions and mitochondrial quality control, are encoded by the nuclear genome and are imported into mitochondria. Hence, the regulation of mitochondrial protein expression and translocation is considered essential for mitochondrial homeostasis. By means of high-throughput RNA sequencing and bioinformatic analysis, non-coding RNAs localized in mitochondria have been generally identified. They are either generated from the mitochondrial genome or the nuclear genome. The mitochondrial non-coding RNAs can directly interact with mitochondrial DNAs or transcripts to affect gene expression. They can also bind nuclear genome-encoded mitochondrial proteins to regulate their mitochondrial import, protein level and combination. Generally, mitochondrial non-coding RNAs act as regulators for mitochondrial processes including oxidative phosphorylation and metabolism. In this review, we would like to introduce the latest research progressions regarding mitochondrial non-coding RNAs and summarize their identification, biogenesis, translocation, molecular mechanism and function.