Free space optical secret key agreement.

Free space optical (FSO) communications are enabling high-speed global wireless networks. Thanks to the highly directional nature of laser beam, they also yield a greater security advantage over radio frequency counterparts. When combined with a scheme of secret key agreement (SKA), FSO-SKA can establish at high speed a symmetric secret key which cannot be decrypted even by unbounded computer resources. Although there have been many theoretical studies on SKA, experimental investigations have been quite lacking, especially on quantifying eavesdropping risks and secret key rates in realistic environment. Here, we report the first full-field implementations of FSO-SKA in a 7.8-km terrestrial link with a probing station, enabling the estimation of eavesdropping risks. We attain the final key rates from 100 kbps to 7.77 Mbps under various atmospheric and beaming conditions even with total losses of 55dB or higher, in which known quantum key distribution schemes attain impractically low key rates.

Free-space optical wiretap channel and experimental secret key agreement in 7.8 km terrestrial link.

Secret key agreement using physical properties of a wireless channel is becoming a promising scheme to establish a secret key between two users, especially in short-distance radio frequency (RF) communications. In this scheme, the existence of codes or key distillation that can make the leaked information to an eavesdropper arbitrarily small can be derived in an information theoretical way, given a priori knowledge on the channel linking a sender (Alice), a legitimate receiver (Bob), and an eavesdropper (Eve), which is called the wiretap channel. In practice, however, it is often difficult for Alice and Bob to get sufficient knowledge on Eve. In this study, we implement a free-space optical wiretap channel in a 7.8 km-terrestrial link and study how to estimate Eve's tapping ability, demonstrating high speed secret key agreement in the optical domain under a certain restricted condition of line-of-sight.

Quantum photonic network and physical layer security.

Quantum communication and quantum cryptography are expected to enhance the transmission rate and the security (confidentiality of data transmission), respectively. We study a new scheme which can potentially bridge an intermediate region covered by these two schemes, which is referred to as quantum photonic network. The basic framework is information theoretically secure communications in a free space optical (FSO) wiretap channel, in which an eavesdropper has physically limited access to the main channel between the legitimate sender and receiver. We first review a theoretical framework to quantify the optimal balance of the transmission efficiency and the security level under power constraint and at finite code length. We then present experimental results on channel characterization based on 10 MHz on-off keying transmission in a 7.8 km terrestrial FSO wiretap channel.This article is part of the themed issue 'Quantum technology for the 21st century'.

Free-space optical channel estimation for physical layer security.

We present experimental data on message transmission in a free-space optical (FSO) link at an eye-safe wavelength, using a testbed consisting of one sender and two receiver terminals, where the latter two are a legitimate receiver and an eavesdropper. The testbed allows us to emulate a typical scenario of physical-layer (PHY) security such as satellite-to-ground laser communications. We estimate information-theoretic metrics including secrecy rate, secrecy outage probability, and expected code lengths for given secrecy criteria based on observed channel statistics. We then discuss operation principles of secure message transmission under realistic fading conditions, and provide a guideline on a multi-layer security architecture by combining PHY security and upper-layer (algorithmic) security.

Exposure to an Extremely-Low-Frequency Magnetic Field Stimulates Adrenal Steroidogenesis via Inhibition of Phosphodiesterase Activity in a Mouse Adrenal Cell Line.

Extremely low-frequency magnetic fields (ELF-MFs) are generated by power lines and household electrical devices. In the last several decades, some evidence has shown an association between ELF-MF exposure and depression and/or anxiety in epidemiological and animal studies. The mechanism underlying ELF-MF-induced depression is considered to involve adrenal steroidogenesis, which is triggered by ELF-MF exposure. However, how ELF-MFs stimulate adrenal steroidogenesis is controversial. In the current study, we investigated the effect of ELF-MF exposure on the mouse adrenal cortex-derived Y-1 cell line and the human adrenal cortex-derived H295R cell line to clarify whether the ELF-MF stimulates adrenal steroidogenesis directly. ELF-MF exposure was found to significantly stimulate adrenal steroidogenesis (p < 0.01-0.05) and the expression of adrenal steroid synthetic enzymes (p < 0.05) in Y-1 cells, but the effect was weak in H295R cells. Y-1 cells exposed to an ELF-MF showed significant decreases in phosphodiesterase activity (p < 0.05) and intracellular Ca2+ concentration (p < 0.01) and significant increases in intracellular cyclic adenosine monophosphate (cAMP) concentration (p < 0.001-0.05) and cAMP response element-binding protein phosphorylation (p < 0.05). The increase in cAMP was not inhibited by treatment with NF449, an inhibitor of the Gs alpha subunit of G protein. Our results suggest that ELF-MF exposure stimulates adrenal steroidogenesis via an increase in intracellular cAMP caused by the inhibition of phosphodiesterase activity in Y-1 cells. The same mechanism may trigger the increase in adrenal steroid secretion in mice observed in our previous study.

Chronic exposure to an extremely low-frequency magnetic field induces depression-like behavior and corticosterone secretion without enhancement of the hypothalamic-pituitary-adrenal axis in mice.

An extremely low-frequency magnetic field (ELF-MF) is generated by power lines and household electrical devices. Many studies have suggested an association between chronic ELF-MF exposure and anxiety and/or depression. The mechanism of these effects is assumed to be a stress response induced by ELF-MF exposure. However, this mechanism remains controversial. In the present study, we investigated whether chronic ELF-MF exposure (intensity, 1.5 mT; [corrected] total exposure, 200 h) affected emotional behavior and corticosterone synthesis in mice. ELF-MF-treated mice showed a significant increase in total immobility time in a forced swim test and showed latency to enter the light box in a light-dark transition test, compared with sham-treated (control) mice. Corticosterone secretion was significantly high in the ELF-MF-exposed mice; however, no changes were observed in the amount of the adrenocorticotropic hormone and the expression of genes related to stress response. Quantification of the mRNA levels of adrenal corticosteroid synthesis enzymes revealed a significant reduction in Cyp17a1 mRNA in the ELF-MF-exposed mice. Our findings suggest the possibility that high intensity and chronic exposure to ELF-MF induces an increase in corticosterone secretion, along with depression- and/or anxiety-like behavior, without enhancement of the hypothalamic-pituitary-adrenal axis.

Effects of a 1.5 T time-varying magnetic field on cell volume regulation of bovine adrenal chromaffin cells in hyposmotic media.

Effects of a time-varying magnetic field on cell volume regulation by hyposmotic stress in cultured bovine adrenal chromaffin cells were examined. Through regulatory volume decrease (RVD), cell volume of chromaffin cells that were incubated in a hypotonic medium initially increased, reached a peak and finally recovered to the initial value. Two hour exposure to a magnetic field and addition of cytochalasin D increased peak value and delayed return to initial value. Intracellular F-actin contents initially decreased but returned to normal levels after 10 sec. Two hour exposure to the magnetic field and addition of cytochalasin D continuously reduced the F-actin content. Results suggest that exposure to the magnetic field stimulated disruption of the actin cytoskeleton and that the disruption delayed the recovery to the volume prior to osmotic stress.

Feed-forward changes in carotid blood flow velocity during active standing.

Orthostatic changes induce temporary loss of circulatory regulation. Feedback systems react to cardiovascular alterations to compensate for the instability. To clarify the existence of anticipatory cardiovascular regulation during active standing, we continuously recorded blood flow velocity (BFV) in the common carotid artery and cerebral blood volume (CBV) in healthy men. The maximum BFV value decreased significantly before standing in the reaction-time condition. The decrease significantly correlated with the change in systolic blood pressure that accompanies upright standing from a supine position. The anticipatory BFV decrease disappeared during self-paced standing, and all BFV parameters significantly declined after the self-paced standing. The CBV recording showed a significant increase in oxyhemoglobin levels before standing in the reaction-time condition. Our study suggests that some feed-forward cardiovascular regulation triggered by central command could be activated before standing, and it may play a functional role in the maintenance of cerebral perfusion during standing.

Effects of exposure to a time-varying 1.5 T magnetic field on the neurotransmitter-activated increase in intracellular Ca(2+) in relation to actin fiber and mitochondrial functions in bovine adrenal chromaffin cells.

BACKGROUND: It has been reported that exposure to electromagnetic fields influences intracellular signal transduction. We studied the effects of exposure to a time-varying 1.5 T magnetic field on membrane properties, membrane cation transport and intracellular Ca(2+) mobilization in relation to signals. We also studied the mechanism of the effect of exposure to the magnetic field on intracellular Ca(2+) release from Ca(2+) stores in adrenal chromaffin cells. METHODS: We measured the physiological functions of ER, actin protein, and mitochondria with respect to a neurotransmitter-induced increase in Ca(2+) in chromaffin cells exposed to the time-varying 1.5 T magnetic field for 2h. RESULTS: Exposure to the magnetic field significantly reduced the increase in [Ca(2+)]i. The exposure depolarized the mitochondria membrane and lowered oxygen uptake, but did not reduce the intracellular ATP content. Magnetic field-exposure caused a morphological change in intracellular F-actin. F-actin in exposed cells seemed to be less dense than in control cells, but the decrease was smaller than that in cytochalasin D-treated cells. The increase in G-actin (i.e., the decrease in F-actin) due to exposure was recovered by jasplakinolide, but inhibition of Ca(2+) release by the exposure was unaffected. CONCLUSIONS AND GENERAL SIGNIFICANCE: These results suggest that the magnetic field-exposure influenced both the ER and mitochondria, but the inhibition of Ca(2+) release from ER was not due to mitochondria inhibition. The effect of eddy currents induced in the culture medium may indirectly influence intracellular actin and suppress the transient increase in [Ca(2+)]i.

Effects of a time-varying strong magnetic field on transient increase in Ca2+ release induced by cytosolic Ca2+ in cultured pheochromocytoma cells.

Exposure of pheochromocytoma (PC 12) cells to a time-varying 1.51 T magnetic field inhibited an increase in the intracellular Ca2+ concentration ([Ca2+]i) induced by addition of caffeine to Ca(2+)-free medium. This inhibition occurred after a 15-min exposure and was maintained for at least 2 h. [Ca2+]i sharply increased in cells loaded with cyclic ADP-ribose, and 2-h exposure significantly suppressed the increase. Addition of ATP induced a transient increase in intracellular Ca2+ release mediated by IP3 receptor, and this increase was strongly inhibited by the exposure. Results indicated that the magnetic field exposure strongly inhibited Ca2+ release mediated by both IP3 and ryanodine receptors in PC 12 cells. However, thapsigargin-induced Ca2+ influx (capacitative Ca2+ entry) across the cell membrane was unaffected. The ATP content was maintained at the normal level during the 2-h exposure, suggesting that ATP hydrolysis was unchanged. Therefore, Mg2+ which is known to be released by ATP hydrolysis and inhibit intracellular Ca2+ release may not relate the exposure-caused inhibition. Eddy currents induced in culture medium appear to change cell membrane properties and indirectly inhibit Ca2+ release from endoplasmic reticulum and other Ca2+ stores in PC 12 cells.

Effects of a time varying strong magnetic field on release of cytosolic free Ca2+ from intracellular stores in cultured bovine adrenal chromaffin cells.

This study was made to explain the mechanisms for the effects of exposure to a time varying 1.51 T magnetic field on the intracellular Ca(2+) signaling pathway. The exposure inhibited an increase in intracellular Ca(2+) concentration ([Ca(2+)](i)) in bovine chromaffin cells induced by addition of bradykinin (BK) to a Ca(2+) free medium. The exposure did not change BK induced production of inositol 1,4,5-trisphosphate (IP(3)). [Ca(2+)](i) was markedly increased in IP(3) loaded cells, and this increase was inhibited by the magnetic field exposure. A similar increase in [Ca(2+)](i) by other drugs, which stimulated Ca(2+) release from intracellular Ca(2+) stores, was again inhibited by the same exposure. However, transmembrane Ca(2+) fluxes caused in the presence of thapsigargin were not inhibited by the magnetic field exposure in a Ca(2+) containing medium. Inhibition of the BK induced increase in [Ca(2+)](i) by the exposure for 30 min was mostly recovered 1 h after exposure ended. Our results reveal that the magnetic field exposure inhibits Ca(2+) release from intracellular Ca(2+) stores, but that BK bindings to BK receptors of the cell membrane and intracellular inositol IP(3) production are not influenced.