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2025
Dynamical decoupling multipulse sequences can be applied to solid-state spins for sensing weak oscillating fields from nearby single nuclear spins. By periodically reversing the probing system's evolution, other noises are counteracted and filtered out over the total evolution. However, the technique is subject to intricate interactions resulting in additional resonant responses, which can be misinterpreted with the actual signal intended to be measured. We experimentally characterize three of these effects present in single nitrogen-vacancy centers in diamond, where we also develop a numerical simulation model without rotating-wave approximation, showing robust correlation to the experimental data. Regarding centers with the N15 nitrogen isotope, we observe that a small misalignment in the bias magnetic field causes the precession of the nitrogen nuclear spin to be sensed by the electronic spin of the center. Another studied case of ambiguous resonances comes from the coupling with lattice C13 nuclei, where we use the echo modulation frequencies to obtain the interaction Hamiltonian and then utilize the latter to simulate multipulse sequences. Finally, we also measure and simulate the effects from the free evolution of the quantum system during finite pulse durations. Due to the large data volume and the strong dependence of these ambiguous resonances with specific experimental parameters, we provide a simulations data set with a user-friendly graphical interface, where users can compare simulations with their own experimental data for spectral disambiguation. Although focused on nitrogen-vacancy centers and dynamical decoupling sequences, these results and the developed model can potentially be applied to other solid-state spins and quantum sensing techniques.
Published by the American Physical Society
2025
- Book : 111(2)
- Pub. Date : 2025
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2025
The discovery of effective cysteine protease inhibitors with crude protein kiwi extracts (CPKEs) has created novel challenges and prospects for pharmaceutical development. Despite extensive research on CPKEs, limited research has been conducted on treating atopic dermatitis (AD). Therefore, the objective of this work was to investigate the anti-inflammatory effects of CPKEs on TNF-α activation in a HaCaT cell model and in a DNCB (1-chloro-2, 4-dinitrochlorobenzene)-induced atopic dermatitis animal model. The molecular weight of the CPKE was determined using SDS-PAGE under non-reducing (17 kDa and 22 kDa) and reducing conditions (25 kDa, 22 kDa, and 15 kDa), whereas gelatin zymography was performed to examine the CPKE’s inhibitory impact on cysteine protease (actinidin and papain) activity. Moreover, the CPKE remains stable at 60 °C, with pH levels varying from 4 to 11, as determined by the azocasein assay. CPKE treatment decreased the phosphorylation of mitogen-activated protein kinase (MAPK) and Akt, along with the activation of nuclear factor-kappa B (NF-κB)-p65 in tumor necrosis factor-α (TNF-α)-stimulated HaCaT cells. Five-week-old BALB/c mice were treated with DNCB to act as an AD-like animal model. The topical application of CPKE to DNCB-treated mice for three weeks substantially decreased clinical dermatitis severity and epidermal thickness and reduced eosinophil infiltration and mast cells into ear and skin tissues. These findings imply that CPKE derived from kiwifruit might be a promising therapy option for inflammatory skin diseases such as AD.- Book : 26(4)
- Pub. Date : 2025
- Page : pp.1534-1534
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2025
Using (2712±14)×106 ψ(2S) events collected with the BESIII detector at the BEPCII collider, we search for the decays ηc(2S)→ωω and ηc(2S)→ωϕ via the process ψ(2S)→γηc(2S). No statistically significant signals are observed. The upper limits of their product branching fractions at the 90% confidence level are determined to be B(ψ(2S)→γηc(2S),ηc(2S)→ωω)<1.04×10−6 and B(ψ(2S)→γηc(2S),ηc(2S)→ωϕ)<1.85×10−7, respectively. We also update the branching fractions of χcJ→ωω and χcJ→ωϕ via the ψ(2S)→γχcJ transition. Their branching fractions are determined to be B(χc0→ωω)=(10.66±0.11±0.57)×10−4, B(χc1→ωω)=(6.43±0.07±0.31)×10−4, B(χc2→ωω)=(8.75±0.08±0.42)×10−4, B(χc0→ωϕ)=(1.18±0.03±0.07)×10−4, B(χc1→ωϕ)=(2.04±0.15±0.11)×10−5, and B(χc2→ωϕ)=(9.58±1.07±0.76)×10−6, where the first uncertainties are statistical and the second are systematic.
Published by the American Physical Society
2025
- Book : 111(3)
- Pub. Date : 2025
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2025
AbstractMast cells (MCs) have a well-established detrimental role in allergic conditions, but they can also impact on diverse malignant conditions, including melanoma. To study the latter, previous studies have mainly evaluated how MCs can influence melanomas/melanoma cells. However, the inverse scenario, i.e., whether melanoma/melanoma cells might impact on MCs has received less attention. Here we investigated this issue and show that melanoma cell-conditioned medium had a strong growth-inhibitory impact on MCs, which was attributed to inhibition of MC proliferation combined with induction of apoptosis. Further, our data indicate that such effects were attributable to melanin present in the melanoma cell-conditioned medium, as similar anti-proliferative effects were seen in response to both free melanin and to melanocores enriched from melanoma-conditioned medium. Melanin did not reduce the expression of MC markers, but was shown to impair MC activation. We also demonstrate that melanin is taken up by MCs, both in cultured MCs andin vivoin melanoma tumors, and it was observed that melanin, after uptake, can be found in the MC nucleus. Further, we show that melanin had marked effects on the nuclear morphology in MCs accompanied by clipping of core histone 3, and it is demonstrated that these events were dependent on translocation of tryptase, a granule-localized protease, into the MC nucleus. Tryptase was also shown to affect the mechanism of melanin-induced cell death. Altogether, the present study outlines a novel mechanism by which melanoma cells can suppress MC function, potentially representing an immunosuppressive mechanism that may influence tumor growth.- Book : ()
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