Ultraviolet writing of channel waveguides in proton-exchanged LiNbO₃

We report on a direct ultraviolet (UV) writing method for the fabrication of channel waveguides at 1.55 µm in LiNbO3 through UV irradiation of surface and buried planar waveguides made by annealed proton exchange and reverse proton exchange. A systematic study of the guidance properties as a function of the UV writing conditions is presented

Macrophage TNF-α mediates parathion-induced airway hyperreactivity in guinea pigs.

Organophosphorus pesticides (OPs) are implicated in human asthma. We previously demonstrated that, at concentrations that do not inhibit acetylcholinesterase activity, the OP parathion causes airway hyperreactivity in guinea pigs as a result of functional loss of inhibitory M2 muscarinic receptors on parasympathetic nerves. Because macrophages are associated with asthma, we investigated whether macrophages mediate parathion-induced M2 receptor dysfunction and airway hyperreactivity. Airway physiology was measured in guinea pigs 24 h after a subcutaneous injection of parathion. Pretreatment with liposome-encapsulated clodronate induced alveolar macrophage apoptosis and prevented parathion-induced airway hyperreactivity in response to electrical stimulation of the vagus nerves. As determined by qPCR, TNF-α and IL-1β mRNA levels were increased in alveolar macrophages isolated from parathion-treated guinea pigs. Parathion treatment of alveolar macrophages ex vivo did not significantly increase IL-1β and TNF-α mRNA but did significantly increase TNF-α protein release. Consistent with these data, pretreatment with the TNF-α inhibitor etanercept but not the IL-1β receptor inhibitor anakinra prevented parathion-induced airway hyperreactivity and protected M2 receptor function. These data suggest a novel mechanism of OP-induced airway hyperreactivity in which low-level parathion activates macrophages to release TNF-α-causing M2 receptor dysfunction and airway hyperreactivity. These observations have important implications regarding therapeutic approaches for treating respiratory disease associated with OP exposures

Processing ultrafast optical signals in broadband telecom systems by means of cascaded quadratic nonlinearities

Quadratic optical nonlinearities offer several attractive features for the implementation of ultra-fast, low-noise and transparent telecom devices. Technological progress has dramatically increased their efficiency, driving a steady move towards practical applications. In this talk we shall discuss the use of cascaded quadratic interactions in LiNbO3 integrated devices for pulse diagnostics, format conversion and signal regeneration in ultra-fast multi-wavelength telecom systems

Processing of telecommunication signals using periodically poled lithium niobate waveguides

This talk reports on processing of high-speed telecommunication signals based on cascaded quadratic nonlinearities in periodically poled lithium niobate (PPLN) waveguides. A strong pump positioned within the acceptance bandwidth of the PPLN device can interact via a cascaded nonlinear process with a second signal, thereby facilitating a switch with a broad optical bandwidth and yielding an output located within the same wavelength band as the inputs. The combination of the PPLN switch with custom-designed optical filtering for pre-conditioning of the signals gives rise to a versatile pulse processing system exhibiting important advantages in terms of compactness and environmental stability. As an example, Fig.1 describes schematically how an optical time-division multiplexed (OTDM) signal can be converted through cascaded second-harmonic generation and difference-frequency generation to a wavelength-division multiplexed (WDM) signal. The experiments that have led to this demonstration will be described in the talk

Nitric oxide-dependent bone marrow progenitor mobilization by carbon monoxide enhances endothelial repair after vascular injury

Carbon monoxide (CO) has emerged as a vascular homeostatic molecule that prevents balloon angioplasty-induced stenosis via antiproliferative effects on vascular smooth muscle cells. The effects of CO on reendothelialization have not been evaluated