High-transmission narrowband ultraviolet filter based on an aluminum laminated nanostructure on glass.

We present an aluminum (Al) laminated nanostructure stacked on a glass substrate to produce highly transmitted narrowband ultraviolet (UV) filters. The laminated nanostructure was mainly composed of an Al nanohole array, and each Al nanohole had a coaxial Al nanoring at the bottom. This UV filter showed a single dominant peak with a high transmission over 50% and a narrow bandwidth less than 80 nm in the 200-400 nm waveband that was achieved based on the synergy of surface plasmon resonance (SPR) and localized surface plasmon resonance (LSPR). The electric field profiles of the laminated nanostructure indicate that SPR selects the transmission wavelength and LSPR contributes to single peak. This narrowband UV filter can be utilized in UV detectors.

Influence of the active layer nanomorphology on device performance for ternary PbS(x)Se(1-x) quantum dots based solution-processed infrared photodetector.

In this paper, the influence of the active layer nanomorphology on device performance for ternary PbS(x)Se(1-x) quantum dot-based solution-processed infrared photodetector is presented. Firstly, ternary PbS(x)Se(1-x) quantum dots (QDs) in various chemical composition were synthesized and the bandgap of the ternary PbS(x)Se(1-x) QDs can be controlled by the component ratio of S/(S + Se), and then field-effect transistor (FET) based photodetectors Au/PbS0.4Se0.6:P3HT/PMMA/Al, in which ternary PbS0.4Se0.6 QDs doped with poly(3-hexylthiophene) (P3HT) act as the active layer and poly(methyl methacrylate) (PMMA) as the dielectric layer, were presented. By changing the weight ratio of P3HT to PbS0.4Se0.6 QDs (K = M(P3HT):M(QDs)) in dichlorobenzene solution, we found that the device with K = 2:1 shows optimal electrical property in dark; however, the device with K = 1:2 demonstrated optimal performance under illumination, showing a maximum responsivity and specific detectivity of 55.98 mA W(-1) and 1.02 × 10(10) Jones, respectively, at low V(DS) = -10 V and V(G) = 3 V under 980 nm laser with an illumination intensity of 0.1 mW cm(-2). By measuring the atomic force microscopy phase images of PbS0.4Se0.6:P3HT films in different weight ratio K, our experimental data show that the active layer nanomorphology has a great influence on the device performance. Also, it provides an easy way to fabricate high performance solution-processed infrared photodetector.

Circ_0050908 up-regulates TRAF3 by sponging miR-324-5p to aggravate myocardial ischemia-reperfusion injury.

BACKGROUND: Aberrant circular RNAs (circRNAs) expression is closely associated with cardiovascular diseases. However, the regulatory functions of circRNAs in myocardial ischemia-reperfusion (I/R) injury remain largely undefined. METHODS: We established myocardial I/R model in vitro by oxygen and glucose deprivation and reperfusion in cardiomyocytes. The expression of circ_0050908, microRNA (miR)-324-5p, and TNF receptor-associated factor (TRAF3) was detected using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. The apoptosis was assayed by flow cytometry and Western blot. The activity of interleukin (IL)-1ß, IL-6, tumor necrosis factor (TNF-α), lactate dehydrogenase (LDH), creatine kinase myocardial band (CK-MB), CK, and superoxide dismutase (SOD) was evaluated using the relative commercial kits. Reactive oxygen species (ROS) detection was conducted using Dihydroethidium (DHE) staining. The interactions between miR-324-5p and circ_0050908 or TRAF3 were determined by dual-luciferase activity, RNA immunoprecipitation (RIP), and pull-down assays. RESULTS: I/R stimulation up-regulated circ_0050908 expression in cardiomyocytes. Functional experiments suggested that circ_0050908 knockdown led to the rescue of apoptosis enhancement, inflammation, and oxidative stress induced by I/R in cardiomyocytes. Mechanistically, circ_0050908 directly targeted miR-324-5p, and miR-324-5p inhibition reversed the inhibitory action of circ_0050908 knockdown on myocardial I/R injury. TRAF3 was verified to be a target of miR-324-5p, and miR-324-5p suppressed I/R-induced apoptosis, inflammatory response, and oxidative stress in cardiomyocytes through TRAF3. Besides that, circ_0050908 could regulate TRAF3 expression by miR-324-5p. CONCLUSION: Circ_0050908 knockdown protects cardiomyocytes against I/R injury by reducing apoptosis, inflammatory response, and oxidative stress through miR-324-5p/TRAF3 axis, revealing a novel therapeutic strategy for preventing myocardial I/R injury.

Inhibition of sphingomyelin synthase 2 relieves hypoxia-induced cardiomyocyte injury by reinforcing Nrf2/ARE activation via modulation of GSK-3ß.

Sphingomyelin synthase 2 (SMS2) is a vital contributor to tissue injury and affects various pathological processes. However, whether SMS2 participates in the modulation of cardiac injury in myocardial infarction has not been determined. This study aimed to evaluate the potential role of SMS2 in the regulation of cardiomyocyte injury induced by hypoxia, an in vitro model for studying myocardial infarction. Our data revealed that SMS2 expression was significantly upregulated in cardiomyocytes in response to hypoxia. Loss-of-function experiments revealed that knockdown of SMS2 markedly restored the viability of cardiomyocytes impaired by hypoxia, and attenuated hypoxia-evoked apoptosis and reactive oxygen species (ROS) generation. In contrast, cardiomyocytes that highly expressed SMS2 were more sensitive to hypoxia-induced injury. Moreover, SMS2 deficiency enhanced the activation of nuclear factor erythroid 2-related factor 2 (Nrf2) signaling through inactivation of glycogen synthase kinase-3ß. Notably, suppression of Nrf2 markedly abrogated SMS2 knockdown-mediated cardioprotective effects on hypoxia-exposed cardiomyocytes. Our results illustrate that downregulation of SMS2 exerts a cardioprotective function by protecting cardiomyocytes from hypoxia-induced apoptosis and oxidative stress through enhancement of Nrf2 activation. Our study indicates a potential role of SMS2 in the modulation of cardiac injury, which may contribute to the progression of myocardial infarction.

Up-regulation of CTRP12 ameliorates hypoxia/re-oxygenation-induced cardiomyocyte injury by inhibiting apoptosis, oxidative stress, and inflammation via the enhancement of Nrf2 signaling.

C1q/TNF-related protein 12 (CTRP12) has been reported to play a key role in coronary artery disease. However, whether CTRP12 plays a role in the regulation of myocardial ischemia-reperfusion injury is not fully understood. The goals of this work were to assess the possible relationship between CTRP12 and myocardial ischemia-reperfusion injury. Here, we exposed cardiomyocytes to hypoxia/re-oxygenation (H/R) to establish an in vitro cardiomyocyte injury model of myocardial ischemia-reperfusion injury. Our results showed that H/R treatment resulted in a decrease in CTRP12 expression in cardiomyocytes. The up-regulation of CTRP12 ameliorated H/R-induced cardiomyocyte injury via the down-regulation of apoptosis, oxidative stress, and inflammation. In contrast, the knockdown of CTRP12 enhanced cardiomyocyte sensitivity to H/R-induced cardiomyocyte injury. Further investigation showed that CTRP12 enhanced the levels of nuclear Nrf2 and increased the expression of Nrf2 target genes in cardiomyocytes exposed to H/R. However, the inhibition of Nrf2 markedly diminished CTRP12-overexpression-mediated cardioprotective effects against H/R injury. Overall, these data indicate that CTRP12 protects against H/R-induced cardiomyocyte injury by inhibiting apoptosis, oxidative stress, and inflammation via the enhancement of Nrf2 signaling. This work suggests a potential role of CTRP12 in myocardial ischemia-reperfusion injury and proposes it as an attractive target for cardioprotection.