Reactive oxygen species (ROS) and antioxidant ingredients are a series of crucial signaling molecules in oxidative stress response. Under some pathological conditions such as traumatic brain injury, ischemia/reperfusion, and hypoxia in tumor, the relative excessive accumulation of ROS could break cellular homeostasis, resulting in oxidative stress and mitochondrial dysfunction. Meanwhile, autophagy is also induced. In this process, oxidative stress could promote the formation of autophagy. Autophagy, in turn, may contribute to reduce oxidative damages by engulfing and degradating oxidized substance. This short review summarizes these interactions between ROS and autophagy in related pathological conditions referred to as above with a focus on discussing internal regulatory mechanisms. The tight interactions between ROS and autophagy reflected in two aspects: the induction of autophagy by oxidative stress and the reduction of ROS by autophagy. The internal regulatory mechanisms of autophagy by ROS can be summarized as transcriptional and post-transcriptional regulation, which includes various molecular signal pathways such as ROS-FOXO3-LC3/BNIP3-autophagy, ROS-NRF2-P62-autophagy, ROS-HIF1-BNIP3/NIX-autophagy, and ROS-TIGAR-autophagy. Autophagy also may regulate ROS levels through several pathways such as chaperone-mediated autophagy pathway, mitophagy pathway, and P62 delivery pathway, which might provide a further theoretical basis for the pathogenesis of the related diseases and still need further research.

Endoplasmic reticulum (ER) stress is a common cellular stress response that is triggered by a variety of conditions that disturb cellular homeostasis, and induces cell apoptosis. Autophagy, an important and evolutionarily conserved mechanism for maintaining cellular homeostasis, is closely related to the apoptosis induced by ER stress. There are common upstream signaling pathways between autophagy and apoptosis induced by ER stress, including PERK/ATF4, IRE1α, ATF6, and Ca . Autophagy can not only block the induction of apoptosis by inhibiting the activation of apoptosis-associated caspase which could reduce cellular injury, but also help to induce apoptosis. In addition, the activation of apoptosis-related proteins can also inhibit autophagy by degrading autophagy-related proteins, such as Beclin-1, Atg4D, Atg3, and Atg5. Although the interactions of different autophagy- and apoptosis-related proteins, and also common upstream signaling pathways have been found, the potential regulatory mechanisms have not been clearly understood. In this review, we summarize the dual role of autophagy, and the interplay and potential regulatory mechanisms between autophagy and apoptosis under ER stress condition.

Endoplasmic reticulum (ER) stress, a common cellular stress response, is closely related to the activation of autophagy that is an important and evolutionarily conserved mechanism for maintaining cellular homeostasis. Autophagy induced by ER stress mainly includes the ER stress-mediated autophagy and ER-phagy. The ER stress-mediated autophagy is characterized by the generation of autophagosomes that include worn-out proteins, protein aggregates, and damaged organelles. While the autophagosomes of ER-phagy selectively include ER membranes, and the double membranes also derive, at least in part, from the ER. The signaling pathways of IRE1α, PERK, ATF6, and Ca are necessary for the activation of ER stress-mediated autophagy, while the receptor-mediated selective ER-phagy degrades the ER is Atg40/FAM134B. The ER stress-mediated autophagy and ER-phagy not only have differences, but also have connections. The activation of ER-phagy requires the core autophagy machinery, and the ER-phagy may be a branch of ER stress-mediated autophagy that selectively targets the ER. However, the determined factors that control the changeover switch between ER stress-mediated autophagy and ER-phagy are largely obscure, which may be associated with the type of cells and the extent of stimulation. This review summarized the crosstalk between ER stress-mediated autophagy and ER-phagy and their signaling networks. Additionally, we discussed the possible factors that influence the type of autophagy induced by ER stress.

Silent information regulator factor 2-related enzyme 1 (sirtuin 1, Sirt1) is a nicotinamide adenine dinucleotide-dependent deacetylase, which can deacetylate histone and non-histone proteins and other transcription factors, and is involved in the regulation of many physiological functions, including cell senescence, gene transcription, energy balance, and oxidative stress. Ischemia/hypoxia injury remains an unresolved and complicated situation in the diseases of ischemia stroke, heart failure, and coronary heart disease, especially among the old folks. Studies have demonstrated that aging could enhance the vulnerability of brain, heart, lung, liver, and kidney to ischemia/hypoxia injury and the susceptibility in old folks to ischemia/hypoxia injury might be associated with Sirt1. In this review, we mainly summarize the role of Sirt1 in modulating pathways against energy depletion and its involvement in oxidative stress, apoptosis, and inflammation under the condition of ischemia/hypoxia.

GeSn lasers enable monolithic integration of lasers on the Si platform using all-group-IV directbandgap materials. Although optically pumped GeSn lasers have made significant progress, the study of the electrically injected lasers has just begun only recently. In this work, we present explorative investigations of electrically injected GeSn heterostructure lasers with various layer thicknesses and material compositions. The cap layer total thickness was varied between 240 and 100 nm. At 10 K, a 240-nm-SiGeSn capped device had a threshold current density Jth = 0.6 kA/cm 2 compared to Jth = 1.4 kA/cm 2 of a device with 100-nm-SiGeSn cap due to an improved modal overlap with the GeSn gain region. Both devices had a maximum operating temperature Tmax = 100 K. Device with cap layers of Si0.03Ge0.89Sn0.08 and Ge0.95Sn0.05, respectively, were also compared. Due to less effective carrier (electron) confinement, the device with a 240-nm-GeSn cap had a higher threshold Jth = 2.4 kA/cm 2 and lower maximum operating temperature Tmax = 90 K, compared to those of the 240-nm-SiGeSn capped device with Jth = 0.6 kA/cm 2 and Tmax = 100 K. In the study of the active region material, the device with Ge0.85Sn0.15 active region had a 2.3 higher Jth and 10 K lower Tmax, compared to the device with Ge0.89Sn0.11 in its active region. This is likely due to higher defect density in Ge0.85Sn0.15 rather than an intrinsic issue. The longest lasing wavelength was measured as 2682 nm at 90 K. The investigations provide guidance to the future structure design of GeSn laser diodes to further improve the performance.

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5Carbon dioxide based oligo(carbonate-ether) diol (CO 2 -polyol) with both carbonate units and ether units in one polymer chain were prepared from copolymerization of CO 2 and propylene oxide (PO) using zinccobalt double metal complex as catalyst, and used to prepare CO 2 based waterborne polyurethane (CO 2 -WPU). The carbonate units in CO 2 -polyol improved the mechanical and oxidation resistance properties of CO 2 -WPU, while the ether units in CO 2 -polyol enhanced the hydrolysis resistance of CO 2 -WPU. The 10 tensile strength of CO 2 -WPU didn't show obvious drop during immersion in 0.25% sodium hydroxide solution, whereas that of oligoesterol based WPU dropped over 50% after 300 min, and lost mechanical property after 520 min immersion. Meanwhile, the retention of tensile strength of CO 2 -WPU was Ca.72% even after 46 h immersion in 6 wt% H 2 O 2 solution, while that was only Ca.32% for oligoetherol based WPU. Moreover, the thermal-mechanical performance of CO 2 -WPU film can be conveniently adjusted by 15 carbonate unit content (CU%) in CO 2 -polyol, i.e., when CU% in CO 2 -polyol increased from 30% to 66%, the glass transition temperature (T g ) increased from -7.8 0 C to 18.8 0 C, accompanied by an increase of tensile strength from 35.6 MPa to 52.2 MPa, a decrease of elongation at break from 630% to 410%. This work suggests that the CO 2 -WPU may be promising alternative for conventional WPU whose oligoetherol and oligoesterol were from fossil resources, and its comprehensive hydrolysis/oxidation 20 resistance may be a bonus unavailable from common oligomerol based WPU. 65 75%. 13 Recently, there is a nice report from Bardow that CO 2polyol may be viable alternative in polyurethane industry from an environmental point of view based on life cycle assessment. 14 We are wondering whether polyol derived from CO 2 and PO is suitable oligomerol for WPU. Up to now, however, there is few 70 reports on such issue.

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