The rapid development of superconducting nanowire single-photon detectors (SNSPDs) over the past decade has led to numerous advances in quantum information technology. The record for the best system detection efficiency (SDE) at an incident photon wavelength of 1550 nm is 93%. This performance was attained from an SNSPD made of amorphous WSi; such SNSPDs are usually operated at sub-Kelvin temperatures. In this study, we fabricated an SNSPD using polycrystalline NbN. Its SDE is 90.2% at 2.1 K for incident photons with a 1550-nm wavelength, and this temperature is accessible with a compact cryocooler. The SDE saturated at 92.1% when the temperature was lowered to 1.8 K. We expect the results lighten the practical and high performance SNSPD to quantum information and other high-end applications. Main textA single-photon detector with high detection efficiency is the key enabling technology for quantum information and various applications, including the test of loophole-free Bell inequality violation 1 , quantum teleportation 2 , measurement-device-independent quantum key distribution 3 , and linear optical quantum computation 4 . Superconducting single-photon detectors outperform their semiconducting counterparts in terms of not only detection efficiency but also dark count rate, timing jitter, and counting rate 5 . In the case of the telecommunication wavelength (1550 nm), the highest system detection efficiency (SDE) greater than 90% has been reported for two types of detectors. One is a transition edge sensor (TES) made of tungsten (W), with an SDE of 95% 6 ; the other is a superconducting nanowire single-photon detector (SNSPD) made of amorphous WSi, with an SDE of 93% 7 . However, because of the low superconducting transition temperature of W and WSi, the requirement of sub-Kelvin cryogenics represents a burden for practical applications. Many studies focused on SNSPDs fabricated using different materials and aiming to obtain a high SDE at higher operating temperatures have been reported [8][9][10][11] ; however, none of these attempts has been successful. Regarding another important parameter, timing jitter, a WSi SNSPD and a W TES have values of approximately 150 ps and 50-100 ns, respectively, which limits their use in
Hepatocellular carcinoma (HCC) is generally acknowledged as the most common primary malignant tumor, and it is known to be resistant to conventional chemotherapy. Wentilactone B (WB), a tetranorditerpenoid derivative extracted from the marine algae-derived endophytic fungus Aspergillus wentii EN-48, has been shown to trigger apoptosis and inhibit metastasis in HCC cell lines. However, the mechanisms of its antitumor activity remain to be elucidated. We report here that WB could significantly induce cell cycle arrest at G2 phase and mitochondrial-related apoptosis, accompanying the accumulation of reactive oxygen species (ROS). Additionally, treatment with WB induced phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), but not p38 MAP kinase. Among the pathway inhibitors examined, only SP600125 (JNK inhibitor) markedly reversedWB-induced apoptosis, and only U0126 (ERK inhibitor) significantly blocked WB-triggered G2 phase arrest. We also found that WB treatment increased both Ras and Raf activation, and transfection of cells with dominant-negative Ras (RasN17) abolishedWB-induced apoptosis and G2 phase arrest in SMMC-7721 cells. Furthermore, the results of inverse docking (INVDOCK) analysis suggested that WB could bind to Ras–GTP, and the direct binding affinity was also confirmed by surface plasmon resonance (SPR). Finally, in vivo, WB suppressed tumor growth in mouse xenograft models. Taken together, these results indicate that WB induced G2/M phase arrest and apoptosis in human hepatoma SMMC-7721 cells via the Ras/Raf/ERK and Ras/Raf/JNK signaling pathways, and this agent may be a potentially useful compound for developing anticancer agents for HCC.
Chemotherapy remains the common therapeutic for patients with lung cancer. Novel, selective antitumor agents are pressingly needed. This study is the first to investigate a different, however, effective antitumor drug candidate Wentilactone A (WA) for its development as a novel agent. In NCI-H460 and NCI-H446 cell lines, WA triggered G2/M phase arrest and mitochondrial-related apoptosis, accompanying the accumulation of reactive oxygen species (ROS). It also induced activation of mitogen-activated protein kinase and p53 and increased expression of p21. When we pre-treated cells with ERK, JNK, p38, p53 inhibitor or NAC followed by WA treatment, only ERK and p53 inhibitors blocked WA-induced apoptosis and G2/M arrest. We further observed Ras (HRas, KRas and NRas) and Raf activation, and found that WA treatment increased HRas–Raf activation. Knockdown of HRas by using small interfering RNA (siRNA) abolished WA-induced apoptosis and G2/M arrest. HRas siRNA also halted Raf, ERK, p53 activation and p21 accumulation. Molecular docking analysis suggested that WA could bind to HRas-GTP, causing accumulation of Ras-GTP and excessive activation of Raf/ERK/p53-p21. The direct binding affinity was confirmed by surface plasmon resonance (SPR). In vivo, WA suppressed tumor growth without adverse toxicity and presented the same mechanism as that in vitro. Taken together, these findings suggest WA as a promising novel, potent and selective antitumor drug candidate for lung cancer.
Low timing jitter is a unique merit of superconducting nanowire single-photon detectors (SNSPDs) for time-correlated applications. Quantitative analysis was performed for the SNSPD system. Aided by an oscilloscope with an optimal signal amplitude, we were able to measure a full width at half-maximum system timing jitter as low as 14.2 ps for a high-switching-current SNSPD using a room-temperature low-noise amplifier. When using a time-correlated single-photon counting module, the system timing jitter was 17.3 ps. The detector's intrinsic timing jitter was estimated at ∼12.0 ps.
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