Analysis of the optimal operation frequency with lowest time-delay jitter for an electrically triggered field-distortion spark gap

This work was stimulated by the assumption that for a gas-filled spark gap closing switch operating at a high repetition frequency, there is an optimal frequency range in which the time-delay jitter reaches a minimum value. The experiments to test this assumption use an electrically triggered, field-distortion spark gap filled with the SF6/N2 gas mixture. The results show that indeed, the time-delay jitter decreases for a range of frequencies for which the filling gas can substantially restore the interelectrode insulation before increasing at a higher operation frequency. The experimental results demonstrate the correctness of the abovepresented assumption: the time-delay jitter of the field-distortion spark gap has its minimum when the unit operates in the repetition frequency range between 20 and 30 Hz. Since the recovery time depends on the gas species and the gap distance, the optimum operation frequency range should also vary depending on the spark-gap distance and the filling gas properties

DataSheet1_Nighttime warming promotes copper translocation from root to shoot of wheat (Triticum aestivum L.) through enlarging root systems.doc

This study aimed to investigate whether and how nighttime warming (NW) influences the copper (Cu) bioaccumulation of wheat (Triticum aestivum L.) under Cu pollution. We examined plant growth, Cu concentration, and antioxidant enzymes of wheat after 6 months of Cu exposure (0, 100, 400, and 800 mg/kg) under NW. The results indicated that, NW of 1.54°C significantly promoted Cu translocation from root to shoot through an increasing root system under increased Cu treatments (p < 0.05). The Cu contents of grains were significantly increased by NW under 800 mg/kg Cu treatment (p < 0.05). NW decreased superoxide dismutase (SOD) activity under increased Cu treatments (p < 0.05). There were significantly negative correlations between biomass and Cu concentrations of the same part under NW (p < 0.05). The root biomass significantly increased by 51% in NW compared with nonnighttime warming (CK) (p < 0.05). These results provided evidence that wheat might respond to NW by altering their roots so that they were larger, thinner, and longer, suggesting that soil Cu translocation from root to shoot would be accelerated resulting from the expanded roots under elevated temperatures, and thus forewarned the food safety risks of climate change in agricultural ecosystem.</p

LY287445 induced the degradation of immunoproteasome subunits through autophagy.

(A) Confirmation of ATG7 gene knock out in macrophages. ATG7 gene was deleted through CRISPR-CAS9 assay in RAW264.7 cells. Clones of gene deletion cells were cultured and detected for protein levels of p62, LC3, ATG7, and intrinsic control GAPDH. The blots were quantified with densitometric values and statistical significance was analyzed. (B) Confirmation of the decrease of p62 protein levels in p62 knock down RAW264.7 cells. The blot was quantified with densitometric values and statistical significance was analyzed. (C) The protein expression of LMP2 and LMP7 in Fig 5A were quantified with densitometric values and statistical significance was analyzed. (D) The protein expression of LMP2, LMP7, and p62 in Fig 5B were quantified with densitometric values and statistical significance was analyzed. (E) The protein expression of LMP2, LMP7, and p62 in Fig 5C were quantified with densitometric values and statistical significance was analyzed. (F) The immune fluorescence micrographs in Fig 5D was quantified by ImageJ. (G) The protein expression of NRB1, Tollip, and p62 in Fig 5E were quantified with densitometric values and statistical significance was analyzed. (H) The protein expression of LMP2 and LMP7 in Fig 5F were quantified with densitometric values and statistical significance was analyzed. *: P P P P S1 Data. (PDF)</p

Controlled Growth of Metal–Organic Framework on Upconversion Nanocrystals for NIR-Enhanced Photocatalysis

Development of MOF-based photocatalysts is intriguing research due to their structural flexibility and tremendous catalytic sites, whereas most MOFs only can take use of UV/visible light and lack of response to NIR light. Herein, we present a facile approach to integrate upconversion nanoparticles (UCNPs) with MOF to build a NIR-responsive composite photocatalyst. The MOF shell with controllable thickness can be grown on the UCNPs, thus exhibiting tunable photocatalytic activities under NIR irradiation. Furthermore, we extend visible absorption of the MOF shell by adding −NH₂ groups so that the composite photocatalysts have a better utilization of UC emissions and sunlight to improve their activities. The developed composite photocatalysts have been characterized by XRD, TEM, PL, etc., and their photocatalytic performances were systematically explored. The formation and working mechanism of the composite photocatalysts were also elucidated

Proteins analyzed by mass spectrometry in RAW264.7 macrophages treated with LPS and LY2874455.

Proteins analyzed by mass spectrometry in RAW264.7 macrophages treated with LPS and LY2874455.</p

LY2874455 suppressed inflammation though autophagy pathway.

(A) Autophagy inhibitor reversed the effect of LY2874455 on ROS-reduction in LPS-stimulated macrophages. RAW264.7 cells were stained with ROS-probe DCFH-DA after treatment with LPS (20 ng/ml), LY2874455 (2 μm), and wortmannin (100 nM) as indicated for 24 h. Quantitative measurement of cellular ROS was performed by flow cytometry. (B, C) Autophagy inhibitor reversed the effect of LY2874455 in LPS-stimulated macrophages. The expression of inflammatory cytokine genes (iNOS and IL-6) was checked by qRT-PCR in RAW264.7 cells treated as (A). (D, E) The expression of inflammatory cytokine IL-6 and iNOS was checked by qRT-PCR in PMs as treated as in (A). (F) Autophagy deficiency reversed the effect of LY2874455 in inflammatory macrophages. WT or ATG7 knock out (ATG7-KO) RAW264.7 cells were treated with LPS (20 ng/ml) and LY2874455 (2 μm) for 24 h. The expression of iNOS and IL-6 was checked by qRT-PCR and expressed as fold changes compared to values in WT cells. (G) p62 knock down reversed the effect of LY2874455 in inflammatory macrophages. Control (sh-CTL, control shRNA) or p62 knockdown (sh-p62, p62-targeting shRNA) RAW264.7 cells were treated with LPS (20 ng/ml) and LY2874455 (2 μm) for 24 h. The expression of iNOS and IL-6 was checked by qRT-PCR and expressed as fold changes compared to values in control cells. (H–J) The enhanced production of proinflammatory factors in autophagy-deficient macrophages was suppressed by immunoproteasome inhibitor ONX-0914. WT or ATG7 knockout (ATG7-KO) RAW264.7 cells treated with LPS (20 ng/ml) and ONX-0914 (1 μm). The expression of iNOS and inflammatory cytokine genes (IL-6 and TNF-α) was checked by qRT-PCR. *: P P P P S1 Data. iNOS, inducible nitric oxide synthase; LPS, lipopolysaccharide; PM, peritoneal macrophage; qRT-PCR, quantitative real-time polymerase chain reaction; ROS, reactive oxygen species; WT, wild type.</p

LY2874455 activated the autophagy process.

(A) Proteasome inhibitor MG132 cannot block the reduction of immunoproteasome subunits induced by LY2874455. Protein levels of LMP2, LMP7, and GAPDH were analyzed in RAW264.7 cells treated with LPS (20 ng/ml), LY2874455 (2 μm), and MG132 (5 μm). The blots were quantified with densitometric values and statistical significance was analyzed. (B, C) Autophagy inhibitors blocked the reduction of immunoproteasome subunits induced by LY2874455. Protein levels of LMP2, LMP7, and GAPDH were analyzed in RAW264.7 cells treated with LPS (20 ng/ml), LY2874455 (2 μm), and autophagy inhibitors chloroquine (CQ, 20 μm) or wortmannin (100 nM). The blots were quantified with densitometric values and statistical significance was analyzed. (D) LY2874455 enhanced autophagy flux. RAW264.7 cells transfected with mCherry-EGFP-LC3 were stimulated with LPS (20 ng/ml) or/and LY2874455 for another 24 h, and the puncta of LC3 in cells was monitored after fixation under a confocal fluorescent microscope. Higher level of mCherry-LC3 signal and lower level of EGFP-LC3 signal (showing red in merge) indicated the stimulated autophagy flux, while the similar signal levels of mCherry-LC3 and GFP-L3 (showing yellow in merge) indicated the blocked autophagy flux. Representative images from 3 replicated experiments were shown. Scale bars: 10 μm. (E) LY2874455 promoted the formation of autophagosomes. RAW264.7 cells treated with control or LY2874455 (2 μm) for 24 h were analyzed by transmission electron microscopy. Autophagosomes were pointed by arrows and representative images from 3 replicated experiments were shown. Scale bars: 1 μm. (F) LY2874455 promoted the autophagic degradation of substrate receptor p62. RAW264.7 cells were treated with LPS (20 ng/ml) and LY2874455 (0.5, 2, 4 μm) with or without Bafilomycin A1 (20 nM) for 24 h and protein levels of p62, LC3, and GAPDH were analyzed by western blot. The blots were quantified with densitometric values and statistical significance was analyzed. (G) Protein levels of p62 and GAPDH were detected by western blot in RAW264.7 cells treated with LY2874455 (2 μm) and LPS (20 ng/ml) and for 24 h. The blot was quantified with densitometric values and statistical significance was analyzed. (H) Protein levels of p62 and GAPDH were detected by western blot in PMs from C57BL/6J mice treated as in (G). The blot was quantified with densitometric values and statistical significance was analyzed. (I) Protein levels of p62 and GAPDH were detected by western blot in BMDMs from C57BL/6J mice treated as in (G). The blot was quantified with densitometric values and statistical significance was analyzed. (J) LY2874455 inhibited the AKT-mTOR signaling. Protein levels of p-mTOR (Ser248), mTOR, p-AKT (Ser473), AKT, and GAPDH were detected by western blot in RAW264.7 cells treated as in (G). The blots were quantified with densitometric values and statistical significance was analyzed. *: P P P P < 0.0001, NS: no statistical difference. BMDM, bone marrow-derived macrophage; LPS, lipopolysaccharide; PM, peritoneal macrophage.</p

LY2874455 suppressed inflammation in LPS-stimulated macrophages.

(A) RAW264.7 cells were incubated with 27 chemicals and stimulated with LPS (20 ng/ml) for 24 h. NO concentration in culture supernatant was measured and shown as fold change. (B) The names of the 27 chemicals. (C, D) Different concentrations of LY2874455 were applied to LPS (20 ng/ml)-treated RAW264.7 cells and cell viabilities and levels of NO were measured. (E–G) The expression of proinflammatory genes (IL-6, TNF-α) and iNOS was checked by qRT-PCR treated with LY2874455 (2 μm) and LPS (20 ng/ml) for 24 h. (H) Protein levels of IL-6, TNF-α, iNOS, and β-actin were detected by western blot in RAW264.7 cells. The blot was quantified with densitometric values and statistical significance was analyzed. (I–K) The expression of proinflammatory genes (IL-6, TNF-α) and iNOS was checked by qRT-PCR in PMs treated with LY2874455 (2 μm) and LPS (20 ng/ml) for 24 h. (L) Protein levels of iNOS and GAPDH were detected by western blot in PM. (M) The blot was quantified with densitometric values and statistical significance was analyzed. (N–P) The expression of proinflammatory genes (IL-6, TNF-α) and iNOS was checked by qRT-PCR in BMDMs treated with LY2874455 (2 μm) and LPS (20 ng/ml) for 24 h. (Q, R) Expression levels of iNOS were detected by in BMDM. The blot was quantified with densitometric values and statistical significance was analyzed. (S, T) The expression of proinflammatory genes (IL-6 and TNF-α) was checked by qRT-PCR in human THP-1 monocytes treated with LY2874455 (2 μm) and LPS (20 ng/ml) for 24 h. Phorbol12-myristate13-acetate (PMA) was used to induce THP-1 monocyte to macrophages. (U, V) The cytokine of IL-6 and TNF-α was detected by elisa in in RAW264.7 cells treated with LY2874455 (2 μm) and LPS (20 ng/ml) for 24 h. (W–Y) The protein expression of IL-6, TNF-α, and iNOS in Fig 1H were quantified with densitometric values and statistical significance was analyzed. (Z–AB) The protein expression of IL-6, TNF-α, and iNOS in S1H Fig were quantified with densitometric values and statistical significance was analyzed. (AC) The protein expression of IKK-β in Fig 1I was quantified with densitometric values and statistical significance was analyzed. (AD–AE) The protein expression of p65 and p-p65 in Fig 1J were quantified with densitometric values and statistical significance was analyzed. (AF) The immune fluorescence micrographs of p65 were quantified in Fig 1K. *: P P P P S1 Data. (PDF)</p

Multifunctional Theranostics for Dual-Modal Photodynamic Synergistic Therapy via Stepwise Water Splitting

Combined therapy using multiple approaches has been demonstrated to be a promising route for cancer therapy. To achieve enhanced antiproliferation efficacy under hypoxic condition, here we report a novel hybrid system by integrating dual-model photodynamic therapies (dual-PDT) in one system. First, we attached core–shell structured up-conversion nanoparticles (UCNPs, NaGdF₄:Yb,Tm@NaGdF₄) on graphitic-phase carbon nitride (<i>g-</i>C₃N₄) nanosheets (one photosensitizer). Then, the as-fabricated nanocomposite and carbon dots (another photosensitizer) were assembled in ZIF-8 metal–organic frameworks through an in situ growth process, realizing the dual-photosensitizer hybrid system employed for PDT via stepwise water splitting. In this system, the UCNPs can convert deep-penetration and low-energy near-infrared light to higher-energy ultraviolet–visible emission, which matches well with the absorption range of the photosensitizers for reactive oxygen species (ROS) generation without sacrificing its efficacy under ZIF-8 shell protection. Furthermore, the UV light emitted from UCNPs allows successive activation of <i>g</i>-C₃N₄ and carbon dots, and the visible light from carbon dots upon UV light excitation once again activate <i>g</i>-C₃N₄ to produce ROS, which keeps the principle of energy conservation thus achieving maximized use of the light. This dual-PDT system exhibits excellent antitumor efficiency superior to any single modality, verified vividly by in vitro and in vivo assay

LY287445 suppressed viral infection- and aging-induced inflammation.

(A–C) LY2874455 inhibited viral infection-induced inflammation. Polyinosinic-polycytidylic acid (poly(I:C)) (50 μg/ml) and LY2874455 (2 μm) were applied to BMDM for 24 h and expression levels of inflammatory cytokines were analyzed qRT-PCR. (D–F) LY2874455 inhibited the bacteria (E. coli) infection-induced inflammation. E. coli and LY2874455 (2 μm) were applied to BMDM for 24 h and expression levels of inflammatory cytokines were analyzed qRT-PCR. (G–K) LY2874455 inhibited H2O2-induced cell aging. NIH3T3 cells were treated with H2O2 (400 μm for 2 h) for induction of cell aging followed by LY2874455 (2 μm) treatment. Representative images of β-GAL staining of the cells were shown (G) and the expression levels of p16 (H) and inflammatory cytokines (I–K) were analyzed by qRT-PCR. (L) The protein expression of IL1β, IL18, and GAPDH were detected by western blot. And the protein expression was quantified with densitometric values and statistical significance was analyzed. *: P P P P S1 Data. (PDF)</p