We report our studies on spectral sensitivity of meander-type, superconducting NbN thin-film single-photon detectors (SPDs), characterized by GHz counting rates of visible and near-infrared photons and negligible dark counts. Our SPDs exhibit experimentally determined quantum efficiencies ranging from ∼0.2% at the 1.55 μm wavelength to ∼70% at 0.4 μm. Spectral dependences of the detection efficiency (DE) at the 0.4 to 3.0-μm-wavelength range are presented. The exponential character of the DE dependence on wavelength, as well as its dependence versus bias current, is qualitatively explained in terms of superconducting fluctuations in our ultrathin, submicron-width superconducting stripes. The DE values of large-active-area NbN SPDs in the visible range are high enough for modern quantum communications.

We have measured the quantum efficiency (QE), GHz counting rate, jitter, and noise-equivalent power (NEP) of nanostructured NbN superconducting single-photon detectors (SSPDs) in the visible to infrared radiation range. Our 3.5-nm-thick and 100- to 200-nm-wide meander-type devices (total area 10×10μm2), operating at 4.2K, exhibit an experimental QE of up to 20% in the visible range and ∼10% at 1.3 to 1.55μm wavelength and are potentially sensitive up to midinfrared (∼10μm) radiation. The SSPD counting rate was measured to be above 2GHz with jitter <18ps, independent of the wavelength. The devices’ NEP varies from ∼10−17W∕Hz1∕2 for 1.55μm photons to ∼10−20W∕Hz1∕2 for visible radiation. Lowering the SSPD operating temperature to 2.3K significantly enhanced its performance, by increasing the QE to ∼20% and lowering the NEP level to ∼3×10−22W∕Hz1∕2, both measured at 1.26μm wavelength.

We studied the effects of airborne particulate matters (PM) on cystic fibrosis (CF) epithelium. We noted that PM enhanced human CF bronchial epithelial apoptosis, activated caspase-9 and PARP-1; and reduced mitochondrial membrane potential. Mitochondrial inhibitors (4,4-diisothiocyanatostilbene-2,2 0 disulfonic acid, rotenone and thenoyltrifluoroacetone) blocked PM-induced generation of reactive oxygen species and apoptosis. PM upregulated pro-apoptotic Bad, Bax, p53 and p21; and enhanced mitochondrial localization of Bax. The antiapoptotic Bcl-2, Bcl-xl, Mcl-1 and Xiap remained unchanged; however, overexpression of Bcl-xl blocked PM-induced apoptosis. Accordingly, we provide the evidence that PM enhances oxidative stress and mitochondrial signaling mediated apoptosis via the modulation of Bcl family proteins in CF.

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