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The improvement of environmental quality is aligned with the betterment of life quality. Poor air quality has a greatest impact on people health, it links to cancer, long-term harm to cardiovascular and respiratory systems. Conversely, safe air quality free of harmful gases such as formaldehyde, volatile organic compounds and carbon monoxide helps to prevent disease and other health problems. The application of information technology can greatly enhance the effectiveness of ensuring good air quality. Therefore, the implementation of environmental quality and harmful gases monitoring system is beneficial to manage indoor air quality. In this work, we built an environment quality monitoring system, which can adjust the indoor air quality and monitor the concentration of formaldehyde, volatile organic compounds and carbon monoxide. If the environment comfort value is out of the standard, the system will give notification if the concentration of harmful gases exceeds the standard, and activates air ventilation and purification devices. With these real-time data, the proposed system can help people make right and timely decisions, and act in time to maintain a healthy environment in the monitored area.

We propose and demonstrate a tunable photonic crystal nanolaser consisting of 1D periodic nanorods wrapped in deformable polydimethylsiloxane. In addition to low-threshold and long-term lasing stability, the nanolaser also displays reproducible and reliable wavelength tuning with a large tunability of 7.7 nm under 1% compression. By further associating with stretching, a very wide wavelength-tunable range of 155 nm that almost spans the entire S+C+L telecommunication bands is successfully demonstrated with a single nanolaser device.

In eukaryotic cells, DNA damage triggers activation of checkpoint signaling pathways that coordinate cell cycle arrest and repair of damaged DNA. These DNA damage responses serve to maintain genome stability and prevent accumulation of genetic mutations and development of cancer. The p38 MAPK was previously implicated in cellular responses to several types of DNA damage. However, the role of each of the four p38 isoforms and the mechanism for their involvement in DNA damage responses remained poorly understood. In this study, we demonstrate that p38γ, but not the other p38 isoforms, contributes to the survival of UV-treated cells. Deletion of p38γ sensitizes cells to UV exposure, accompanied by prolonged S phase cell cycle arrest and increased rate of apoptosis. Further investigation reveal that p38γ is essential for the optimal activation of the checkpoint signaling caused by UV, and for the efficient repair of UV-induced DNA damage. These findings have established a novel role of p38γ in UV-induced DNA damage responses, and suggested that p38γ contributes to the ability of cells to cope with UV exposure by regulating the checkpoint signaling pathways and the repair of damaged DNA.

ZnO deposited on sapphire substrate is investigated as a function of growth temperature in the range 350∼650 °C. The surface morphology of ZnO structures changes significantly with increasing growth temperature. Though ZnO crystal quality and optical property can be improved under high growth temperature, ZnO is inclined to form nanostructures. Therefore, we propose the repeated growing and annealing (RGA) growth mode as a reliable and reproducible way for the growth of ZnO film. The RGA growth mode is performed at a growth temperature of 450 °C for 8 min, an anneal temperature of 650 °C for 20 min, and repeatedly switched between growing and annealing. Meanwhile, we compare the effects of annealing under Ar, N2, and O2, and found that a low resistivity of 3.4 × 10−3Ω cm and a high mobility of 85.2 cm2V−1s−1can be obtained annealing under N2.

Positive selection of thymocytes during T-cell development is mediated by T-cell receptor (TCR)–activated signals. For different mitogen-activated protein kinases (MAPKs) activated by TCR complex, a selective involvement of extracellular signal–regulated kinase, but not p38 MAPK, in positive selection has been suggested. Using transgenic mice with dominant-negative mutation of both MAP kinase kinase 3 (MMK3) and MKK6, we obtained mice with different extents of inhibition of p38 MAPK activation. Partial inhibition of p38 MAPK impaired CD4−CD8− thymocyte development and T-cell proliferation, but not positive selection. Interference with thymocyte positive selection was observed in mice with effective suppression of p38 MAPK. Our results suggest that, in addition to early thymocyte development, p38 is involved in positive selection.

Positive selection of thymocytes during T-cell development is mediated by T-cell receptor (TCR)–activated signals. For different mitogen-activated protein kinases (MAPKs) activated by TCR complex, a selective involvement of extracellular signal–regulated kinase, but not p38 MAPK, in positive selection has been suggested. Using transgenic mice with dominant-negative mutation of both MAP kinase kinase 3 (MMK3) and MKK6, we obtained mice with different extents of inhibition of p38 MAPK activation. Partial inhibition of p38 MAPK impaired CD4−CD8−thymocyte development and T-cell proliferation, but not positive selection. Interference with thymocyte positive selection was observed in mice with effective suppression of p38 MAPK. Our results suggest that, in addition to early thymocyte development, p38 is involved in positive selection.

Apoptosis of lymphocytes is triggered by different stimuli through the induced expression of Fas and Fas ligand (FasL). Using T cell activation-induced Fas/FasL expression as a model system, we observed a differential regulation of the induction of Fas and FasL. cAMP inhibited activation-induced apoptosis by an effective suppression of TCR-coupled FasL expres sion. In contrast, cAMP weakly interfered with activation-induced Fas expression, and the remaining Fas molecules on cAMP-treated T cells still mediated apoptosis. Among the major transcription elements on the FasL promoter, the activation of NF-κB, but not of NF-AT and AP-1, was suppressed by cAMP. The prominent role of NF-κB was further demonstrated by a better activation of the FasL promoter and an elevated expression of FasL induced by p65 (RelA) overexpression than those induced by AP-1 or NF-AT. Our results demonstrate the essential role of NF-κB for the expression of the death receptor ligand FasL, and suggest a direct link between NF-κB activation and the expression of FasL. NF-κB may be the common mediator in the induction of FasL through TCR activation and by various stress stimuli.

Ceramide has been suggested as the secondary messenger mediating the apoptotic signal for Fas engagement. By using different inhibitors, we demonstrated here that ceramide is unlikely a mediator of Fas-initiated apoptosis. First, cAMP prevented cell death induced by ceramide but not by Fas. Second, ceramide-triggered, but not Fas-triggered, apoptosis was antagonized by the free radical scavenger C60. Third, the metal chelator pyrrolidinedithiocarbamate suppressed ceramide-initiated DNA fragmentation but had no effect on the Fas-induced cell death. Fourth, the SAPK/ERK kinase dominant negative mutant, which attenuated ceramide-induced cell death, did not prevent Fas-induced apoptosis. Finally, activation of NF-κB inhibited ceramide-induced but not Fas-initiated apoptosis. The fact that many antagonists of ceramide-induced apoptosis could not suppress Fas-mediated cell death clearly indicates that ceramide is not the mediator for Fas-initiated apoptotic signal.

Ceramide has been suggested as the secondary messenger mediating the apoptotic signal for Fas engagement. By using different inhibitors, we demonstrated here that ceramide is unlikely a mediator of Fas-initiated apoptosis. First, cAMP prevented cell death induced by ceramide but not by Fas. Second, ceramide-triggered, but not Fas-triggered, apoptosis was antagonized by the free radical scavenger C60. Third, the metal chelator pyrrolidinedithiocarbamate suppressed ceramide-initiated DNA fragmentation but had no effect on the Fas-induced cell death. Fourth, the SAPK/ERK kinase dominant negative mutant, which attenuated ceramide-induced cell death, did not prevent Fas-induced apoptosis. Finally, activation of NF-κB inhibited ceramide-induced but not Fas-initiated apoptosis. The fact that many antagonists of ceramide-induced apoptosis could not suppress Fas-mediated cell death clearly indicates that ceramide is not the mediator for Fas-initiated apoptotic signal.