Solvent engineering for scalable fabrication of perovskite/silicon tandem solar cells in air.

Perovskite/silicon tandem solar cells hold great promise for realizing high power conversion efficiency at low cost. However, achieving scalable fabrication of wide-bandgap perovskite (~1.68 eV) in air, without the protective environment of an inert atmosphere, remains challenging due to moisture-induced degradation of perovskite films. Herein, this study reveals that the extent of moisture interference is significantly influenced by the properties of solvent. We further demonstrate that n-Butanol (nBA), with its low polarity and moderate volatilization rate, not only mitigates the detrimental effects of moisture in air during scalable fabrication but also enhances the uniformity of perovskite films. This approach enables us to achieve an impressive efficiency of 29.4% (certified 28.7%) for double-sided textured perovskite/silicon tandem cells featuring large-size pyramids (2-3 µm) and 26.3% over an aperture area of 16 cm2. This advance provides a route for large-scale production of perovskite/silicon tandem solar cells, marking a significant stride toward their commercial viability.

Reducing Perovskite/C60 Interface Losses via Sequential Interface Engineering for Efficient Perovskite/Silicon Tandem Solar Cell.

Wide-bandgap (WBG) perovskite solar cells hold tremendous potential for realizing efficient tandem solar cells. However, nonradiative recombination and carrier transport losses occurring at the perovskite/electron-selective contact (e.g. C60 ) interface present significant obstacles in approaching their theoretical efficiency limit. To address this, a sequential interface engineering (SIE) strategy that involves the deposition of ethylenediamine diiodide (EDAI2 ) followed by sequential deposition of 4-Fluoro-Phenethylammonium chloride (4F-PEACl) is implemented. The SIE technique synergistically narrows the conduction band offset and reduces recombination velocity at the perovskite/C60 interface. The best-performing WBG perovskite solar cell (1.67 eV) delivers a power conversion efficiency (PCE) of 21.8% and an impressive open-circuit voltage of 1.262 V. Moreover, through integration with double-textured silicon featuring submicrometer pyramid structures, a stabilized PCE of 29.6% is attained for a 1 cm2 monolithic perovskite/silicon tandem cell (certified PCE of 29.0%).

Induced oxidative stress and apoptosis by 1-bromopropane in SH-SY5Y cells correlates with inhibition of Nrf2 function.

In this study, we established SH-SY5Y human neuroblastoma cells as an in vitro model to investigate whether oxidative stress and the nuclear erythroid-2 related factor 2 (Nrf2) signaling pathway are associated with 1-bromopropane (1-BP) -induced nerve cell injury. We identified that 1-BP exhibited neurotoxicity mainly through oxidant-based processes in SH-SY5Y cells, as reactive oxygen species, malondialdehyde levels, and 8-hydroxy-2' -deoxyguanosine significantly increased, while superoxide dismutase activity decreased. Furthermore, Nrf2 translocation from the cytosol to the nucleus was inhibited, as was downstream protein expression of the Nrf2-regulated genes HO-1 and Bcl-2. Activation of caspase-9 and -3 increased, and apoptosis was observed. Vitamin C alleviated 1-BP-induced apoptosis by decreasing oxidative stress and activating the Nrf2 signaling pathway. Knockdown of Nrf2 in SH-SY5Y cells increased 1-BP-induced reactive oxygen species production and cell apoptosis, and inhibited HO-1 and Bcl-2 protein expression, while overexpression of Nrf2 alleviated these processes. These findings suggest that 1-BP-induced oxidative stress and apoptosis in SH-SY5Y cells are associated with Nrf2 function inhibition.

Optical Simulation-Aided Design and Engineering of Monolithic Perovskite/Silicon Tandem Solar Cells.

Monolithic perovskite/c-Si tandem solar cells have attracted enormous research attention and have achieved efficiencies above 30%. This work describes the development of monolithic tandem solar cells based on silicon heterojunction (SHJ) bottom- and perovskite top-cells and highlights light management techniques assisted by optical simulation. We first engineered (i)a-Si:H passivating layers for (100)-oriented flat c-Si surfaces and combined them with various (n)a-Si:H, (n)nc-Si:H, and (n)nc-SiOx:H interfacial layers for SHJ bottom-cells. In a symmetrical configuration, a long minority carrier lifetime of 16.9 ms was achieved when combining (i)a-Si:H bilayers with (n)nc-Si:H (extracted at the minority carrier density of 1015 cm-3). The perovskite sub-cell uses a photostable mixed-halide composition and surface passivation strategies to minimize energetic losses at charge-transport interfaces. This allows tandem efficiencies above 23% (a maximum of 24.6%) to be achieved using all three types of (n)-layers. Observations from experimentally prepared devices and optical simulations indicate that both (n)nc-SiOx:H and (n)nc-Si:H are promising for use in high-efficiency tandem solar cells. This is possible due to minimized reflection at the interfaces between the perovskite and SHJ sub-cells by optimized interference effects, demonstrating the applicability of such light management techniques to various tandem structures.

Plasma superoxide dismutase activity in relation to disability in activities of daily living and objective physical functioning among Chinese older adults.

BACKGROUND: This study aimed to examine the associations of plasma superoxide dismutase (SOD) activity, an indicator of oxidative stress, with disability in activities of daily living (ADL) and objective physical functioning among Chinese older adults. METHODS: We used cross-sectional data of 2223 older adults (≥65 years, including 1505 adults≥80 years) from the 2011/2012 main survey of the Chinese Longitudinal Healthy Longevity Survey (CLHLS) and the 2012 biomarker sub-study. Plasma SOD activity was assessed by the T-SOD assay kit based on the hydroxylamine method. Outcomes included ADL disability and disability in three objective physical tasks (standing up from a chair, picking up a book from the floor, and turning around 360°). Logistic regression models were used to examine the associations of plasma SOD activity with outcomes. RESULTS: After controlling for age and sex, compared with participants in the lowest quartile group of SOD activity, those in the highest quartile group had 31% lower odds of ADL disability (odds ratio [OR]: 0.69; 95%CI: 0.48, 0.98); 60% lower odds of disability in standing up from a chair (OR: 0.40; 95%CI: 0.25, 0.63); and 57% lower odds of disability in picking up a book from a floor (OR: 0.43; 95%CI: 0.28, 0.65). The results did not change substantially after controlling for additional covariates. We did not observe statistically significant age and sex differences. CONCLUSIONS: Overall, plasma SOD activity was associated with subjectively and objectively measured disability in Chinese older adults, highlighting the potential of SOD activity to serve as a biomarker of physical functioning.

1-Bromopropane-induced apoptosis in OVCAR-3 cells via oxidative stress and inactivation of Nrf2.

The bromoalkane, 1-bromopropane (1-BP), may damage the reproductive system though oxidative stress, while the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) plays an important role in regulating intracellular antioxidant levels against oxidative stress. This study explored the role of oxidative stress and the Nrf2 signaling pathway in mediating the reproductive toxicity of 1-BP using the ovarian carcinoma cell line OVCAR-3 as an in vitro model of the human ovary. OVCAR-3 cells were treated with 1, 5, 10 and 15 mM 1-BP. After 24 h, the cellular reactive oxygen species and malondialdehyde concentrations significantly increased, while the superoxide dismutase activity decreased; translocation of Nrf2 from the cytosol to the nucleus as well as downstream protein expression of Nrf2-regulated genes heme oxygenase-1 and Bcl-2 was inhibited. Apoptosis was also observed, accompanied by increased caspase-3 and caspase-9 activity. The antioxidant vitamin C alleviated 1-BP-induced apoptosis by inhibiting caspase activity activating the Nrf2 signaling pathway. These findings suggested that 1-BP induced oxidative stress and apoptosis in OVCAR-3 cells through inactivation of Nrf2 signaling.

High-Mobility Hydrogenated Fluorine-Doped Indium Oxide Film for Passivating Contacts c-Si Solar Cells.

Broadband transparent conductive oxide layers with high electron mobility (µe) are essential to further enhance crystalline silicon (c-Si) solar cell performances. Although metallic cation-doped In2O3 thin films with high µe (>60 cm2 V-1 s-1) have been extensively investigated, the research regarding anion doping is still under development. In particular, fluorine-doped indium oxide (IFO) shows promising optoelectrical properties; however, they have not been tested on c-Si solar cells with passivating contacts. Here, we investigate the properties of hydrogenated IFO (IFO:H) films processed at low substrate temperature and power density by varying the water vapor pressure during deposition. The optimized IFO:H shows a remarkably high µe of 87 cm2 V-1 s-1, a carrier density of 1.2 × 1020 cm-3, and resistivity of 6.2 × 10-4 Ω cm. Then, we analyzed the compositional, structural, and optoelectrical properties of the optimal IFO:H film. The high quality of the layer was confirmed by the low Urbach energy of 197 meV, compared to 444 meV obtained on the reference indium tin oxide. We implemented IFO:H into different front/back-contacted solar cells with passivating contacts processed at high and low temperatures, obtaining a significant short-circuit current gain of 1.53 mA cm-2. The best solar cell shows a conversion efficiency of 21.1%.

Mono(2-ethylhexyl) phthalate induces apoptosis in p53-silenced L02 cells via activation of both mitochondrial and death receptor pathways.

Mono(2-ethylhexyl) phthalate (MEHP) is one of the main metabolites of di(2-ethylhexyl) phthalate. The evidence shows that DEHP may exert its toxic effects primarily via MEHP, which is 10-fold more potent than its parent compound in toxicity in vitro. MEHP-induced apoptosis is mediated by either p53-dependent or -independent pathway. However, the detailed mechanism of its toxicity remains unclear. In this study, immortalized normal human liver cell line L02 was chosen, as an in vitro model of nonmalignant liver, to elucidate the role of p53 in MEHP-induced apoptosis. The cells were treated with MEHP (6.25, 12.50, 25.00, 50.00, and 100.00 µM) for 24 and 36 h, then small interfering RNA (siRNA) was used to specifically silence p53 gene of L02 cells. The results indicated that MEHP caused oxidative DNA damage and apoptosis in L02 cells were associated with the p53 signaling pathway. Further study found that MEHP (50.00 and 100.00 µM) induced apoptosis in p53-silenced L02 cells, along with the up-regulations of Fas and FasL proteins as well as increased the Bax/Bcl-2 ratio and Caspase 3, 8, and 9 activities. Additionally, both FasL inhibitor (AF-016) and Caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp- fluoromethylketone (Z-VAD-FMK) could prevent the cell apoptosis induced by MEHP. The findings suggested that MEHP-induced apoptosis in L02 cells involving a Caspases-mediated mitochondrial signaling pathway and/or death receptor pathway. p53 was not absolutely necessary for MEHP-induced L02 cell apoptosis.

[Investigation of non-ionizing radiation hazards from physiotherapy equipment in 16 medical institutions].

OBJECTIVE: To investigate the non-ionizing radiation hazards from physiotherapy equipment in medical institutions and to explore feasible control measures for occupational diseases. METHODS: On-site measurement and assessment of ultra-high-frequency radiation, high-frequency electromagnetic field, microwave radiation, and laser radiation were carried out in 16 medical institutions using the methods in the Measurement of Physical Agents in Workplace (GBZ/T189-2007). RESULTS: All the investigated medical institutions failed to take effective protective measures against non-ionizing radiation. Of the 17 ultra-short wave therapy apparatus, 70.6%, 47.1%, and 17.64% had a safe intensity of ultra-high-frequency radiation on the head, chest, and abdomen, respectively. Of the 4 external high-frequency thermotherapy apparatus, 100%, 75%, and 75%had a safe intensity of high-frequency electromagnetic field on the head, chest, and abdomen, respectively. In addition, the intensities of microwave radiation and laser radiation produced by the 18 microwave therapy apparatus and 12 laser therapeutic apparatus met national health standards. CONCLUSION: There are non-ionizing radiation hazards from physiotherapy equipment in medical institutions, and effective prevention and control measures are necessary.

MEHP-induced oxidative DNA damage and apoptosis in HepG2 cells correlates with p53-mediated mitochondria-dependent signaling pathway.

In the present study, the effects of MEHP on human hepatocellular liver carcinoma HepG2 cells were investigated. The results showed that MEHP-induced oxidative DNA damage in the treatment groups (≥ 25.00 µM) at 24h after treatment and in the 100.00 µM treatment group at 36 h after treatment (p < 0.05 or p < 0.01). At 36 h after treatment, MEHP at higher concentrations (≥ 25.00 µM) resulted in a decrease in ATP level, and an increase in the protein levels of cytochrome c and Smac/DIABLO in the cytosol as well as the percentage of apoptotic cells. The activation of caspase-9 and -3 and the expression of the selected apoptosis-related proteins, p53, PUMA, NOXA, Bax and Bcl-2 were also induced. Furthermore, vitamin C, a scavenger of reactive oxygen species, attenuated MEHP-induced apoptosis. These findings indicated that MEHP induced oxidative DNA damage and apoptosis in HepG2 cells, and p53 and its downstream proteins were involved in mitochondria- and caspase-mediated apoptosis induced by MEHP.

Mono-2-ethylhexyl phthalate induced loss of mitochondrial membrane potential and activation of Caspase3 in HepG2 cells.

L02 and HepG2 cells were exposed to mono-(2-ethylhexyl) phthalate (MEHP) at concentrations of 6.25-100µM. After 48h treatment, MEHP decreased HepG2 cell viability in a concentration-dependent manner and L02 cell viability in the 50 and 100µM groups (p<0.01). Furthermore, at 24 and 48h after treatment, MEHP decreased the glutathione levels of HepG2 cells in all treatment groups and in the ΔΨ(m) in L02 and HepG2 cells with MEHP≥25µM (p<0.05 or p<0.01). At 24h after treatment, MEHP induced activation of caspase3 in all treated HepG2 and L02 cells (p<0.05 or p<0.01) except the 100µM MEHP treatment group. The increase in the Bax to Bcl-2 ratio suggests that Bcl-2 family involved in the control of MEHP-induced apoptosis in these two cell types. The data suggest that MEHP could induce apoptosis of HepG2 cells through mitochondria- and caspase3-dependent pathways.

Benzo(a)pyrene induces p73 mRNA expression and necrosis in human lung adenocarcinoma H1299 cells.

p53 can mediate DNA damage-induced apoptosis in various cell lines treated with Benzo(a)pyrene (BaP). However, the potential role of p73, one of the p53 family members, in BaP-induced apoptotic cell death remains to be determined. In this study, normal fetal lung fibroblasts (MRC-5) and human lung adenocarcinoma cells (H1299, p53-null) were treated with BaP at concentrations of 8, 16, 32, 64, and 128 µM for 4 and 12 h. The oxidative stress status, extent of DNA damage, expression of p53, p73, mdm2, bcl-2, and bax at the mRNA and protein levels, and the percentages of apoptosis and/or necrosis were assessed. In the two BaP-treated cell lines, we observed increased malondialdehyde (MDA) formation and decreased superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity at 4 h after the treatment; furthermore, at the time points of 4 and 12 h, we observed extremely high levels of DNA damage. In addition, at 4 h after the treatment, BaP had induced necrosis in MRC-5 and H1299 cells, but it had inhibited apoptosis in MRC-5 cells (P < 0.01 for all). Furthermore, in BaP-treated H1299 cells, only the p73 mRNA level was up-regulated. The results suggested that BaP-induced DNA damage could trigger a shift from apoptotic cell death toward necrotic cell death and that necrotic cell death is independent of p53 and p73 in these cell lines. Future studies are needed to investigate the time course of changes in the type of BaP-induced cell death in more cell lines.

Benzo(a)pyrene-induced mitochondrial dysfunction and cell death in p53-null Hep3B cells.

Benzo(a)pyrene (BaP) has been shown to induce apoptosis and necrosis in various cell types. However, the effect of BaP on mitochondria function and p73, and their possible roles in BaP-induced cell death have not been well studied. This study focused on mitochondria-mediated cell death and the occurrence of p73 protein accumulation in BaP-treated human hepatoma Hep3B (p53-null) cells. We found that BaP (8, 16, 32 and 64µM) induced early necrosis at 12h and delayed apoptosis at 24h. BaP dramatically induced ethoxyresorufin-O-deethylase activity and led to significant increase in oxidative stress at early time points (6 and 12h). Necrotic cell death was concurrent with loss of mitochondrial membrane potential, decrease in the ATP level and activities of Na(+)/K(+)-ATPase and Ca(2+)/Mg(2+)-ATPase. However, these changes were reversed in the process of apoptosis. In addition, after BaP treatment, c-Jun N-terminal kinase (JNK) and Bax were activated during apoptosis and no change in p73 protein level was observed. These results revealed that the cells with mitochondria dysfunction and ATP depletion underwent necrosis at early time point and apoptosis afterward when they recovered from mitochondrial dysfunction and ATP depletion. Activation of JNK and Bax possibly contributed to BaP-induced apoptosis.

Mitochondrial dysfunction and transactivation of p53-dependent apoptotic genes in BaP-treated human fetal lung fibroblasts.

Benzo(a)pyrene (BaP) has been shown to be an inducer of apoptosis. However, mechanisms involved in BaP-induced mitochondrial dysfunction are not well-known. In this study, human fetal lung fibroblasts cells were treated with BaP (8, 16, 32, 64 and 128 µM) for 4 and 12 h. Cell viability, intracellular level of reactive oxygen species (ROS), total antioxidant capacity (T-AOC), mitochondrial membrane potential (ΔΨ(m)) and cytochrome c release were determined. Changes in transcriptional levels of p53-dependent apoptotic genes (p53, APAF1, CASPASE3, CASPASE9, NOXA and PUMA) were measured. At time point of 4 h, BaP induced the intracellular ROS generation in 64 (p < .05) and 128 µM BaP groups (p < .01) but decreased the T-AOC activities in 32, 64 (p < .05 for both) and 128 µM BaP groups (p < .01). At time point of 12 h, ΔΨ(m) significantly decreased in ≥32 µM BaP groups (p < .05 for all). Amount of mitochondrial cytochrome c significantly increased in 128 µM BaP group (p < .01). Transcriptional levels of CASPASE3, CASPASE9, APAF1 and PUMA were up-regulated in all BaP groups (p < .05 for all) and in ≥32 µM groups for NOXA (p < .05). But only in 16 µM BaP group a relatively little expression of p53 mRNA was observed (p < .05). The results indicate that in the earlier period BaP promoted the generation of excessive ROS and subsequently the mitochondrial depolarization, whereas transactivations of the p53-dependent apoptotic genes were significantly induced at the later period.

Mechanism for alpha-MnO2 nanowire-induced cytotoxicity in Hela cells.

Alpha-Manganese dioxide (alpha-MnO2) nanowires are used as electrode materials to significantly enhance the performance of lithium batteries. In this study, we investigate the nanotoxicity of alpha-MnO2 nanowires toward Hela cells. The alpha-MnO2 nanowires, which were successfully synthesized using the hydrothermal approach, can induce cytotoxicity dose-dependently in Hela cells. The accumulation of reactive oxygen species (ROS) and depletion of glutathione (GSH) are also observed in the nanowire-treated cells. In addition, comet assays and cell nucleus morphology show that both DNA damage and cell apoptosis occur in the nanowires exposure group. Based on these results, a mechanism for alpha-MnO2 nanowire-induced cytotoxicity in Hela cells, which involves the accumulation of ROS, formation of oxidative stress, DNA oxidative damage and cell apoptosis, is proposed. This investigation may provide a fundamental insight to understand the nanotoxicity of wire-shaped nanomaterials.

Intense red light emission of Eu3+-doped LiGd(PO3)4 for mercury-free lamps and plasma display panels application.

In order to obtain a suitable red phosphor for mercury-free lamps and plasma display panels (PDPs), samples of trivalent europium-activated polyphosphate LiGd(PO(3))(4):Eu(3+) (LGP:Eu(3+)) were prepared by a solid-state reaction technique at high temperature. The vacuum ultraviolet (VUV)-visible spectroscopic properties were investigated. Because the phosphor LiGd(1-x)Eu(x)(PO(3))(4) for x = 0.50 shows broad and strong absorption in VUV region and exhibits intensive emission under 147/172 nm excitation in comparison with the PDP commercial red phosphor (Y, Gd)BO(3):Eu(3+), it is considered to be a promising red phosphor for mercury-free lamps and plasma display panels application.

Efficient emission-tunable VUV phosphors Na(2)GdF(2)PO(4):Tb(3+).

In this paper, we present the VUV-vis spectroscopic properties of Na(2)GdF(2)PO(4):Tb(3+) phosphors prepared at 700 degrees C. The phosphors exhibit some favorable luminescence characteristics such as intensive and broad absorption near 147/172 nm, high bright emission in whole doping concentration, and tunable chromaticity coordinates from blue to whitish and further to yellowish-green range by changing the doping concentration of Tb(3+). As a result, this series of phosphors Na(2)Gd(1-x)Tb(x)F(2)PO(4) can be considered as promising candidates for plasma display panels (PDPs) and Hg-free fluorescent tubes application.