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This paper focuses on how the electron temperature and other plasma properties affect optical emission and CO2 conversion in CO2 plasma. Such plasma-mediated reactions can enable efficient CO2 reuse. We study CO2 and CO plasmas generated by inductively coupled radiofrequency power (30–300 W) at low pressures (6–400 Pa). By varying the argon admixture, we can study the effect of the electron temperature, Te, on the conversion and emission properties using optical emission spectroscopy, mass spectrometry, and electrical probe measurements. Importantly, we can observe several parameters simultaneously: Te, CO2 conversion, chemiluminescence from CO2, and dissociation products and optical emission from several atomic and CO transitions and from the C2 Swan system. On the basis of these results, we establish a correlation between Te, the CO2 conversion, and the optical emission spectra. A low Te enhances CO2 conversion and Swan band emission. In contrast with published studies, our results show that the CO2 and C2 vibrations are not in local equilibrium. This means that the vibrational temperatures of CO2 and C2 should differ.

Recently, several dysregulated microRNAs (miRNAs) have been identified in organisms exposed to graphene oxide (GO). However, their biological functions and mechanisms of the action are still largely unknown. Here, we investigated the molecular mechanism of mir-231 in the regulation of GO toxicity using in vivo assay system of Caenorhabditis elegans. We found that GO exposure inhibited the expression of mir-231::GFP in multiple tissues, in particular in the intestine. mir-231 acted in intestine to regulate the GO toxicity and overexpression of mir-231 in intestine caused a susceptible property of nematodes to GO toxicity. smk-1 encoding a homologue to mammalian SMEK functioned as a targeted gene for mir-231 and was also involved in the intestinal regulation of GO toxicity. Mutation of smk-1 gene induced a susceptible property to GO toxicity, whereas the intestinal overexpression of smk-1 resulted in a resistant property to GO toxicity. Moreover, mutation of smk-1 gene suppressed the resistant property of mir-231 mutant to GO toxicity. In nematodes, SMK-1 further acted upstream of the transcriptional factor DAF-16/FOXO in insulin signaling pathway to regulate GO toxicity. Therefore, mir-231 may encode a GO-responsive protection mechanism against the GO toxicity by suppressing the function of the SMK-1 - DAF-16 signaling cascade in nematodes.

Graphene oxide (GO) has been shown to cause multiple toxicities in various organisms. However, the underlying molecular mechanisms for GO-induced shortened longevity are still unclear. We employed Caenorhabditis elegans to investigate the possible involvement of insulin signaling pathway in the control of GO toxicity and its underlying molecular mechanisms. Mutation of daf-2, age-1, akt-1, or akt-2 gene induced a resistant property of nematodes to GO toxicity, while mutation of daf-16 gene led to a susceptible property of nematodes to GO toxicity, suggesting that GO may dysregulate the functions of DAF-2/IGF-1 receptor, AGE-1, AKT-1 and AKT-2-mediated kinase cascade and DAF-16/FOXO transcription factor. Genetic interaction analysis suggested the involvement of signaling cascade of DAF-2-AGE-1-AKT-1/2-DAF-16 in the control of GO toxicity on longevity. Moreover, intestinal RNA interference (RNAi) analysis demonstrated that GO reduced longevity by affecting the functions of signaling cascade of DAF-2-AGE-1-AKT-1/2-DAF-16 in the intestine. DAF-16 could also regulate GO toxicity on longevity by functioning upstream of SOD-3, which encodes an antioxidation system that prevents the accumulation of oxidative stress. Therefore, intestinal insulin signaling may encode two different molecular mechanisms responsible for the GO toxicity in inducing the shortened longevity. Our results highlight the key role of insulin signaling pathway in the control of GO toxicity in organisms.

The magnetic quantum criticality in strongly correlated electron systems has been considered to be closely related with the occurrence of unconventional superconductivity. Control parameters such as magnetic field, pressure or chemical doping are frequently used to externally tune the quantum phase transition for a deeper understanding. Here we report the research of a field-induced quantum phase transition using conventional bulk physical property measurements in the archetypal antiferromagnet CeCu2Ge2, which becomes superconductive under a pressure of about 10 GPa with Tc ~ 0.64 K. We offer strong evidence that short-range dynamic correlations start appearing above a magnetic field of about 5 T. Our demonstrations of the magnetic instability and the field-induced quantum phase transition are crucial for the quantum criticality, which may open a new route in experimental investigations of the quantum phase transition in heavy-fermion systems.

Lactic acid bacteria (LAB) is safe and useful for food and feed fermentation. We employed Caenorhabditis elegans to investigate the possible beneficial effect of LAB (Lactobacillus bulgaricus) pretreatment against toxicity of graphene oxide (GO) and the underlying mechanisms. LAB prevented GO toxicity on the functions of both primary and secondary targeted organs in wild-type nematodes. LAB blocked translocation of GO into secondary targeted organs through intestinal barrier by maintaining normal intestinal permeability in wild-type nematodes. Moreover, LAB prevented GO damage on the functions of both primary and secondary targeted organs in exposed nematodes with mutations of susceptible genes (sod-2, sod-3, gas-1 and aak-2) to GO toxicity by sustaining normal intestinal permeability. LAB also sustained the normal defecation behavior in both wild-type nematodes and nematodes with mutations of susceptible genes. Therefore, the beneficial role of LAB against GO toxicity under different genetic backgrounds may be due to the combinational effects on intestinal permeability and defecation behavior. Moreover, the beneficial effects of LAB against GO toxicity was dependent on the function of ACS-22, homologous to mammalian FATP4 to mammalian FATP4. Our study provides highlight on establishment of pharmacological strategy to protect intestinal barrier from toxicity of GO.

Cu is widely used in the back contact formation of CdTe thin film solar cells. However, Cu is easily to diffuse from the back contact into the CdTe absorber layer and even to the cell junction interface CdS/CdTe. This phenomenon is generally believed to be the main factor affecting the CdTe solar cell stability. In this study Cu was intentionally doped in CdS thin film to study its effect on the microstructural, optical and electrical properties of the CdS material. Upon Cu doping, the VCd− and the surface-state-related photoluminescence emissions were dramatically decreased/quenched. The presence of Cu atom hindered the recrystallization/coalescence of the nano-sized grains in the as-deposited CdS film during the air and the CdCl2 annealing. CdTe thin film solar cell fabricated with Cu-doped CdS window layers demonstrated much decreased fill factor, which was induced by the increased space-charge recombination near the p-n junction and the worsened junction crystalline quality. Temperature dependent current-voltage curve measurement indicated that the doped Cu in the CdS window layer was not stable at both room and higher temperatures.